Showing papers on "Intraperitoneal injection published in 2010"
TL;DR: Although this paper provides initial information on the potential reproductive and developmental toxicity of manufactured nanomaterials, further studies, especially in vivo, using characterized nanoparticles, relevant routes of administration, and doses closely reflecting expected levels of exposure are needed.
233 citations
TL;DR: The utility of IP injection is demonstrated by injecting glucose and monitoring the rise in blood glucose level and its subsequent return to normal and as stress is known to increase blood glucose in teleost fish, a comparison of blood glucose levels in vehicle-injected and non-injection adults is compared and it is shown that the procedure does not cause a significant rise inBlood glucose levels.
Abstract: A convenient method for chemically treating zebrafish is to introduce the reagent into the tank water, where it will be taken up by the fish. However, this method makes it difficult to know how much reagent is absorbed or taken up per fish. Some experimental questions, particularly those related to metabolic studies, may be better addressed by delivering a defined quantity to each fish, based on weight. Here we present a method for intraperitoneal (IP) injection into adult zebrafish. Injection is into the abdominal cavity, posterior to the pelvic girdle. This procedure is adapted from veterinary methods used for larger fish. It is safe, as we have observed zero mortality. Additionally, we have seen bleeding at the injection site in only 5 out of 127 injections, and in each of those cases the bleeding was brief, lasting several seconds, and the quantity of blood lost was small. Success with this procedure requires gentle handling of the fish through several steps including fasting, weighing, anesthetizing, injection, and recovery. Precautions are required to minimize stress throughout the procedure. Our precautions include using a small injection volume and a 35G needle. We use Cortland salt solution as the vehicle, which is osmotically balanced for freshwater fish. Aeration of the gills is maintained during the injection procedure by first bringing the fish into a surgical plane of anesthesia, which allows slow operculum movements, and second, by holding the fish in a trough within a water-saturated sponge during the injection itself. We demonstrate the utility of IP injection by injecting glucose and monitoring the rise in blood glucose level and its subsequent return to normal. As stress is known to increase blood glucose in teleost fish, we compare blood glucose levels in vehicle-injected and non-injected adults and show that the procedure does not cause a significant rise in blood glucose.
178 citations
TL;DR: An interesting phenomenon is discovered indicating that the absorption of BBR by oral administration has a limit, therefore, explaining the difficulty in obtaining an LD(50) of B BR for i.g. injection.
169 citations
TL;DR: Systemic phage administration was more effective than inhalational administration, suggesting that circulating phages have better access to bacteria in lungs than do topical phages.
Abstract: The therapeutic potential of bacteriophages (phages) in a mouse model of acute Burkholderia cenocepacia pulmonary infection was assessed. Phage treatment was administered by either intranasal inhalation or intraperitoneal injection. Bacterial density, macrophage inflammatory protein 2 (MIP-2), and tumor necrosis factor alpha (TNF-alpha) levels were significantly reduced in lungs of mice treated with intraperitoneal phages (P < .05). No significant differences in lung bacterial density or MIP-2 levels were found between untreated mice and mice treated with intranasal phages, intraperitoneal ultraviolet-inactivated phages, or intraperitoneal lambda phage control mice. Mock-infected mice treated with phage showed no significant increase in lung MIP-2 or TNF-alpha levels compared with mock-infected/mock-treated mice. We have demonstrated the efficacy of phage therapy in an acute B. cenocepacia lung infection model. Systemic phage administration was more effective than inhalational administration, suggesting that circulating phages have better access to bacteria in lungs than do topical phages.
132 citations
TL;DR: The bilateral pain reduction after unilateral toxin application and the effectiveness of lower dose with the faster onset after the intrathecal injection suggest the involvement of the central nervous system in the antinociceptive action of BTX-A in painful diabetic neuropathy.
117 citations
TL;DR: It is shown that there are strain differences in mice in their susceptibility to AA nephropathy, and that AAI exerted the strongest nephrotoxic effect in mice, while AAIVa and ALI caused no neph rotoxicity in this experimental system.
Abstract: Aristolochic acids (AA), present in Aristolochia plants, are the toxin responsible for Chinese herbs nephropathy (CHN), a rapidly progressive tubulointerstitial nephritis (TIN). To clarify the mechanisms of the development of CHN, we tried to induce TIN in mice using AA. Three strains of inbred mice, BALB/c, C3H/He and C57BL/6, received 2.5 mg kg(-1) of AA or AA sodium salt (AANa) daily by intraperitoneal or oral administration, 5 days a week for 2 weeks. Serum and renal tissue were obtained at sacrifice. Twelve-hour urine samples were individually collected in a metabolic cage at one-week intervals. In the AA-injected groups, severe tubular injury, with the appearance of acute tubular necrosis, and rare cell infiltration into the interstitium, were seen in BALB/c mice. C3H/He mice also developed TIN with prominent cell infiltration into the interstitium and interstitial fibrosis. In C57BL/6 mice, only mild and focal tubulointerstitial changes were seen. Serum creatinine and blood urea nitrogen increased in BALB/c and C3H/He mice. Immunofluorescent study revealed no deposition of immune components in kidneys. In the AANa-treated groups, TIN was also seen in all groups, but even more severe tubulointerstitial changes were induced by intraperitoneal injection. Further examination using purified AAI, AAII, AAIVa and aristolactam I (ALI) revealed that AAI induced strong nephrotoxicity in mice, and that AAII resulted in mild nephrotoxicity. However, AAIVa and ALI caused no nephrotoxicity in this experimental system. There are strain differences in mice in their susceptibility to AA nephropathy. AAI exerted the strongest nephrotoxic effect in mice.
116 citations
TL;DR: PBN alleviated mechanical allodynia induced by paclitaxel in rats, and data show that PBN given on days 7 through 15 after the first pac litaxel injection prevented the development of chemotherapy-induced neuropathic pain.
Abstract: Background: Paclitaxel is a widely used chemotherapeutic drug for breast and ovarian cancer. Unfortunately, it induces neuropathic pain, which is a dose-limiting side effect. Free radicals have been implicated in many neurodegenerative diseases. The current study tests the hypothesis that a free radical scavenger plays an important role in reducing chemotherapy-induced neuropathic pain. Methods: Neuropathic pain was induced by intraperitoneal injection of paclitaxel (2 mg/kg) on four alternate days (days 0, 2, 4, and 6) in male Spraue-Dawley rats. Phenyl N-tert-butylnitrone (PBN), a free radical scavenger, was administered intraperitoneally as a single dose or multiple doses before or after injury. Mechanical allodynia was measured by using von Frey filaments. Results: The administration of paclitaxel induced mechanical allodynia, which began to manifest on days 7-10, peaked within 2 weeks, and plateaued for at least 2 months after the first paclitaxel injection. A single injection or multiple intraperitoneal injections of PBN ameliorated paclitaxel-induced pain behaviors in a dose-dependent manner. Further, multiple administrations of PBN starting on day 7 through day 15 after the first injection of paclitaxel completely prevented the development of mechanical allodynia. However, an intraperitoneal administration of PBN for 8 days starting with the first paclitaxel injection did not prevent the development of pain behavior. Conclusions: This study clearly shows that PBN alleviated mechanical allodynia induced by paclitaxel in rats. Furthermore, our data show that PBN given on days 7 through 15 after the first paclitaxel injection prevented the development of chemotherapy-induced neuropathic pain. This clearly has a clinical implication.
108 citations
TL;DR: It could be concluded that quercetin, a flavonoid with antioxidant properties, exerts its beneficial antidiabetic effects in rats by exerting its beneficial anti-inflammatory effects.
Abstract: Quercetin (QE), one of natural flavanoid group, was widely distributed as a secondary metabolite in plant kingdom. It has been believed that oxidative stress plays a role in the pathogenesis of diabetes mellitus (DM). The aim of the present study was the evaluation of possible effects of QE on blood glucose and antioxidant enzymes in experimental streptozotocin (STZ)-induced diabetes in rats. STZ was injected intraperitoneally with single dose of 50 mg/kg for diabetes induction. QE (15 mg/kg bw day, intraperitoneal (i.p.) injection) was injected for 3 days prior to STZ administration; these injections were continued to the end of the study (for 25 days). Glucose tolerance test and random plasma glucose were done for all animals. Cellular antioxidant enzymes such as glutathione peroxidase (GSHPx), superoxide dismutase (SOD) and catalase (CAT) activities were measured in pancreatic homogenates. Quercetin had no effect on plasma glucose level of normal animals but its pre- treatment was able to prevent diabetes induced by single intraperitoneal injection of streptozocintreated rats. Antioxidant enzyme activity significantly decreased in STZ induced diabetic group. QE treatment significantly increased the antioxidant enzyme activities. It could be concluded that quercetin, a flavonoid with antioxidant properties, exerting its beneficial antidiabetic effects.
108 citations
TL;DR: The potential application of cetuximab-conjugated magneto-fluorescent nanoparticles (MFSN-Ctx) for the detection of EGFR-expressing colon cancer using in vivo imaging approaches is demonstrated.
101 citations
TL;DR: Data show that DFO inhibits inflammation and atherosclerosis in experimental mice, providing the proof-of-concept for an important role of iron in atherogenesis, whether eliminating excess iron is a useful adjunct for the prevention or treatment of atheros sclerosis in humans.
Abstract: Vascular inflammation and monocyte recruitment are initiating events in atherosclerosis that have been suggested to be caused, in part, by iron-mediated oxidative stress and shifts in the intracellular redox environment of vascular cells. Therefore, the objective of this study was to investigate whether the intracellular iron chelator, desferrioxamine (DFO), reduces inflammation and atherosclerosis in experimental mice. Treatment of C57BL/6J mice with DFO (daily intraperitoneal injection of 100 mg/kg body weight for two weeks) strongly inhibited lipopolysaccharide-induced increases of soluble cellular adhesion molecules and monocyte chemoattractant protein-1 (MCP-1) in the serum and activation of the redox-sensitive transcription factors, nuclear factor-kappaB and activator protein-1, in the aorta. Furthermore, treatment of apolipoprotein E-deficient (apoE-/-) mice with DFO (100 mg/kg, intraperitoneal, daily for 10 weeks) attenuated aortic atherosclerotic lesion development by 26% (P < 0.05). DFO treatment of apoE-/- mice also lowered serum levels of MCP-1 and gene expression of proinflammatory and macrophage markers in the aorta and heart, in parallel with increased protein expression of the transferrin receptor in the heart and liver. In contrast, DFO treatment had no effect on serum cholesterol and triglyceride levels. These data show that DFO inhibits inflammation and atherosclerosis in experimental mice, providing the proof-of-concept for an important role of iron in atherogenesis. Whether eliminating excess iron is a useful adjunct for the prevention or treatment of atherosclerosis in humans remains to be investigated.
99 citations
TL;DR: It is suggested that ZER reduces oxidative stress, inhibits proliferation, induces mitochondria-regulated apoptosis, thus minimising DEN/AAF-induced carcinogenesis in rat liver, and has great potential in the treatment of liver cancers.
TL;DR: Results reveal a pivotal role for ceramide biosynthesis in obesity, metabolic syndrome, and associated kidney damage.
Abstract: The present study tested a hypothesis that excess accumulation of sphingolipid, ceramide, its metabolites, or a combination contributes to the development of obesity and associated kidney damage. Liquid chromatography/mass spectrometry analysis demonstrated that C57BL/6J mice on the high-fat diet (HFD) had significantly increased plasma total ceramide levels compared with animals fed a low-fat diet (LFD). Treatment of mice with the acid sphingomyelinase (ASMase) inhibitor amitriptyline significantly attenuated the HFD-induced plasma ceramide levels. Corresponding to increase in plasma ceramide, the HFD significantly increased the body weight gain, plasma leptin concentration, urinary total protein and albumin excretion, glomerular damage index, and adipose tissue ASMase activity compared with the LFD-fed mice. These HFD-induced changes were also significantly attenuated by treatment of mice with amitriptyline. In addition, the decline of plasma glucose concentration after an intraperitoneal injection of insulin (0.15 U/kg b.wt.) was more sustained in mice on the HFD with amitriptyline than on the HFD alone. Intraperitoneal injection of glucose (3 g/kg b.wt.) resulted in a slow increase followed by a rapid decrease in the plasma glucose concentration in LFD and HFD plus amitriptyline-treated mice, but such blood glucose response was not observed in HFD-fed mice. Immunofluorescence analysis demonstrated a decrease in the podocin and an increase in the desmin in the glomeruli of HFD-fed mice compared with the LFD and HFD plus amitriptyline-treated mice. In conclusion, our results reveal a pivotal role for ceramide biosynthesis in obesity, metabolic syndrome, and associated kidney damage.
TL;DR: The present data suggest that H(2)S attenuates LPS-induced cognitive impairment through reducing the overproduction of pro-inflammatory mediators via inhibition of NF-kappaB pathways in rats.
Abstract: The present study investigated the effect of sodium hydrosulfide (NaHS), a H 2 S donor, on cognitive impairment and neuroinflammatory changes induced by bilateral intracerebroventricular injections of LPS at a dose of 10 μg/rat. Rats received 5 mg/kg NaHS or volume-matched vehicle administration by intraperitoneal injection 3 days before LPS injection then for 9 days once daily. Morris water maze was used to detect the cognitive function. Compared to the sham-treated rats, LPS injection significantly prolonged the mean escape latency in the navigation test ( P P 2 S level but increased pro-inflammatory mediators (i.e., TNF-α, TNFR1, degradation of IκB-α and thereafter activation of NF-κB) in hippocampus. However, these effects of LPS were significantly ameliorated with NaHS treatment ( P vs vehicle-treated group). The present data suggest that H 2 S attenuates LPS-induced cognitive impairment through reducing the overproduction of pro-inflammatory mediators via inhibition of NF-κB pathways in rats. This study sets the stage for exploring a novel H 2 S releasing agent for preventing or retarding the development or progression of neurological disorders such as Alzheimer's disease.
TL;DR: A role for FoxO1 in the antineoplastic effect of CR through the induction of genes responsible for protection against oxidative and genotoxic stress is suggested.
Abstract: The FoxO transcription factors may be involved in the antiaging effect of calorie restriction (CR) in mammals. To test the hypothesis, we used FoxO1 knockout heterozygotic (HT) mice, in which the FoxO1 mRNA level was reduced by 50%, or less, of that in wild-type (WT) mouse tissues. The WT and HT mice were fed ad libitum (AL) or 30% CR diets from 12 weeks of age. Aging- and CR-related changes in body weight, food intake, blood glucose, and insulin concentrations were similar between the WT and HT mice in the lifespan study. The response to oxidative stress, induced by intraperitoneal injection of 3-nitropropionic acid (3-NPA), was evaluated in the liver and hippocampus at 6 months of age. Several of the selected FoxO1-target genes for cell cycle arrest, DNA repair, apoptosis, and stress resistance were up-regulated in the WT-CR tissues after 3-NPA injection, while the effect was mostly diminished in the HT-CR tissues. Of these gene products, we focused on the nuclear p21 protein level in the liver and confirmed its up-regulation only in the WT-CR mice in response to oxidative stress. The lifespan did not differ significantly between the WT and HT mice in AL or CR conditions. However, the antineoplastic effect of CR, as indicated by reduced incidence of tumors at death in the WT-CR mice, was mostly abrogated in the HT-CR mice. The present results suggest a role for FoxO1 in the antineoplastic effect of CR through the induction of genes responsible for protection against oxidative and genotoxic stress.
Journal Article•
TL;DR: In this article, the liver- protective effects of hydroalcoholic extract of Allium hirtifolium on liver enzymes level in rats with alloxan-induced diabetes mellitus was investigated.
Abstract: BACKGROUND: Diabetes mellitus is one of the most common endocrine disorders accompa- nied with many metabolic syndromes. Use of herbal medicines has always been an option to treat a great number of diseases such as diabetes and its complications. In this study the liver- protective effects of hydroalcoholic extract of Allium hirtifolium on liver enzymes level in rats with alloxan-induced diabetes mellitus was investigated. METHODS: Thirty five male rats were randomly divided into five groups of seven; group 1: nondiabetic control, group 2: diabetic control, group 3: diabetic treated with shallot extract (0.1 g/kg), group 4: diabetic rats treated with shallot extract (1 g/kg), and group 5: diabetic treated with glibenclamide (0.6 mg/kg). Using intraperitoneal (IP) injection of alloxan monohydrate, diabetes mellitus was induced in rats. Diabetic rats were treated with intraperitoneal injection for 4 weeks. At the end of the experimental period fasting blood samples were collected. RESULTS: Statistical analysis of the data indicated that hydroalcoholic extract of shallot can significantly decrease serum contents of liver enzymes (ALP, AST, and ALT) in treated groups. In most cases, the effectiveness of the extract on reduction of these enzymes is more than gli- benclamide. CONCLUSION: Antioxidant compounds in the extract may recover liver damages caused by free radicals in diabetic rats.
TL;DR: It is revealed that hMSCs can exert prosurvival effects on renal cells in vitro and in vivo, suggests a paracrine contribution for kidney protective abilities of h MSCs delivered ip, and supports their clinical potential in AKI.
Abstract: Acute kidney injury (AKI) can occur from the toxic side-effects of chemotherapeutic agents such as cisplatin. Bone marrow-derived mesenchymal stromal cells (MSCs) have demonstrated wide therapeutic potential often due to beneficial factors they secrete. The goal of this investigation was to evaluate in vitro the effect of human MSCs (hMSCs) secretome on cisplatin-treated human kidney cells, and in vivo the consequence of hMSCs intraperitoneal (ip) implantation in mice with AKI. Our results revealed that hMSCs-conditioned media improved survival of HK-2 human proximal tubular cells exposed to cisplatin in vitro. This enhanced survival was linked to increased expression of phosphorylated Akt (Ser473) and was reduced by a VEGF-neutralizing antibody. In vivo testing of these hMSCs established that ip administration in NOD-SCID mice decreased cisplatin-induced kidney function impairment, as demonstrated by lower blood urea nitrogen levels and higher survival. In addition, blood phosphorous and amylase levels were also significantly decreased. Moreover, hMSCs reduced the plasma levels of several inflammatory cytokines/chemokines. Immunohistochemical examination of kidneys showed less apoptotic and more proliferating cells. Furthermore, PCR indicated the presence of hMSCs in mouse kidneys, which also showed enhanced expression of phosphorylated Akt. In conclusion, our study reveals that hMSCs can exert prosurvival effects on renal cells in vitro and in vivo, suggests a paracrine contribution for kidney protective abilities of hMSCs delivered ip, and supports their clinical potential in AKI.
TL;DR: PO-TRF was found to be more effective hypoglycemic and nephroprotective agent in DN than RBO- TRF.
Journal Article•
TL;DR: This animal study suggests that pretreatment with RGSE protects against gentamicin-induced acute kidney injury as evident on tissue histology, however, this was not accompanied with significant improvement in biochemical markers of kidney injury.
Abstract: INTRODUCTION. This study was designed to determine the protective effect of red grape seed extract (RGSE) on gentamicin-induced nephrotoxicity in rats. MATERIALS AND METHODS. Thirty male Wistar rats were divided into 3 groups to receive RGSE, for 60 days followed by intraperitoneal injection of saline solution (as placebo) for 8 days (group 1); RGSE followed by gentamicin for 8 days (group 2); and gentamicin without pre-medication of RGSE (group 3). Oral RGSE, 40 mg/kg/d, and intraperitoneal injection of gentamicin, 100 mg/kg/d, were administered in these groups of rats. Blood and urine samples were collected on days 0 and 68 of the study. Then, the kidneys were removed for pathologic examination. RESULTS. On day 68, serum creatinine and blood urea nitrogen concentrations were highest in group 3, which was significantly higher than in group 1 (P = .001 and P = .004, respectively), while slightly higher than in group 2 (P = .30 and P = .50, respectively). Fractional excretion of sodium was not significantly different between the three groups. Histopathological evaluation showed that rats in group 3 had significantly higher degrees of severe acute tubular necrosis and interstitial mononuclear cell infiltration than the rats in groups 1 and 2 (P < .001). CONCLUSIONS. This animal study suggests that pretreatment with RGSE protects against gentamicin-induced acute kidney injury as evident on tissue histology. However, this was not accompanied with significant improvement in biochemical markers of kidney injury.
TL;DR: Curcumin can protect the liver and kidney from the damage caused by acetaminophen overdose and has the potential to be used in a combination therapy with NAC, significantly decreasing the therapeutic dose of NAC and therefore its side-effects.
TL;DR: It is interesting to note that post-treatment of vitamin E showed more protection in the kidney compared to pre-treatment, and in brain tissue, partial protection was observed on oxidative stress parameters.
TL;DR: 111In-NLS-trastuzumab is a promising radioimmunotherapeutic agent that could be effective for treatment of HER2-overexpressing breast cancer in humans.
Abstract: 111In-nuclear localization sequence-trastuzumab is a radioimmunotherapeutic agent consisting of trastuzumab modified with NLS peptides (CGYGPKKKRKVGG) and labeled with the Auger electron emitter 111In. Our objectives were to evaluate the tumor growth–inhibitory properties and normal-tissue toxicity of 111In-NLS-trastuzumab in mice after intraperitoneal administration. Methods: The pharmacokinetics of 111In-NLS-trastuzumab after intravenous (tail vein) or intraperitoneal injection in BALB/c mice were compared. Normal-tissue toxicity was determined in BALB/c mice at 2 wk after intraperitoneal injection of 3.7–18.5 MBq (4 mg/kg) of 111In-NLS-trastuzumab by monitoring body weight, histopathologic examination of tissues, and hematology (white blood cell, platelet, red blood cell, and hemoglobin) or clinical biochemistry (alanine transaminase and creatinine) parameters. A no-observable-adverse-effect-level (NOAEL) dose was defined. Athymic mice bearing subcutaneous MDA-MB-361 or MDA-MB-231 human breast cancer xenografts (5.0 × 105 or 0.5 × 105HER2/cell, respectively) were treated with a single NOAEL dose or 2 doses administered intraperitoneally and separated by 2 wk. Control groups were administered 111In-trastuzumab, trastuzumab, nonspecific 111In-NLS-human IgG (hIgG), or normal saline. Results: The bioavailability of 111In-NLS-trastuzumab after intraperitoneal injection was 0.7. The NOAEL dose was 9.25 MBq (4 mg/kg); doses greater than or equal to 18.5 MBq decreased white blood cell or platelet counts, and doses of 27.7 MBq decreased red blood cell counts. There was no increase in alanine transaminase or creatinine at any doses tested. There were no morphologic changes to the liver, kidneys, heart, or spleen or loss of body weight. A single dose of 111In-NLS-trastuzumab (9.25 MBq)—compared with mice receiving 111In-trastuzumab, trastuzumab, 111In-NLS-hIgG, or normal saline—significantly slowed the rate of growth of MDA-MB-361 tumors over 60 d (0.014 d−1 vs. 0.033 d−1, 0.046 d−1, 0.030 d−1, and 0.061 d−1, respectively; P 140 d vs. 96 and 84 d, respectively; P
TL;DR: Genomic analysis provided further evidence that mitochondria are the primary target of doxorubicin-induced oxidative damage that leads to cardiomyopathy and the primary site of cardioprotective action by dexrazoxane.
Abstract: The antineoplastic anthracycline doxorubicin can induce a dose-dependent cardiomyopathy that limits the total cumulative dose prescribed to cancer patients. In both preclinical and clinical studies, pretreatment with dexrazoxane, an intracellular iron chelator, partially protects against anthracycline-induced cardiomyopathy. To identify potential additional cardioprotective treatment strategies, we investigated early doxorubicin-induced changes in cardiac gene expression. Spontaneously hypertensive male rats (n = 47) received weekly intravenous injections of doxorubicin (3 mg/kg) or saline 30 min after pretreatment with dexrazoxane (50 mg/kg) or saline by intraperitoneal injection. Cardiac samples were analyzed 24 h after the first (n = 20), second (n = 13), or third (n = 14) intravenous injection on days 1, 8, or 15 of the study, respectively. Rats receiving three doses of doxorubicin had minimal myocardial alterations that were attenuated by dexrazoxane. Cardiac expression levels of genes associated with the Nrf2-mediated stress response were increased after a single dose of doxorubicin, but not affected by cardioprotectant pretreatment. In contrast, an early repressive effect of doxorubicin on transcript levels of genes associated with mitochondrial function was attenuated by dexrazoxane pretreatment. Dexrazoxane had little effect on gene expression by itself. Genomic analysis provided further evidence that mitochondria are the primary target of doxorubicin-induced oxidative damage that leads to cardiomyopathy and the primary site of cardioprotective action by dexrazoxane. Additional strategies that prevent the formation of oxygen radicals by doxorubicin in mitochondria may provide increased cardioprotection.
TL;DR: Overall, among the different sized neutral liposomes investigated, the 1000 nm vesicles seemed to be the most optimal, achieving a greater peritoneal level and retention, and their organ to blood AUC ratio was the lowest.
TL;DR: The effects of four common anesthesia procedures on plasma concentrations of glucose, lactate, non-esterified fatty acids, and corticosterone in blood obtained from a previously implanted jugular vein (JV) catheter are compared.
TL;DR: This study investigated the beneficial effects of asiatic acid—a triterpenoid compound—preserved beta mass and mitigated hyperglycemia in streptozocin‐induced diabetic rats.
Abstract: Background
Type 1 diabetes is a chronic condition in which the pancreas produces little or no insulin due to the loss or dysfunction of pancreatic beta cells. This study investigated the beneficial effects of asiatic acid—a triterpenoid compound—preserved beta mass and mitigated hyperglycemia in streptozocin-induced diabetic rats.
Methods
Diabetes mellitus was induced in adult male Wistar rats by a single intraperitoneal injection of streptozocin (60 mg/kg body weight). The diabetic rats were divided into untreated and asiatic acid (25 mg/kg) groups. Controls were intraperitoneal injection with citrate buffer. Blood glucose level, plasma insulin, and pancreas immunohistochemistry analysis were examined after a 2-week experimental period. AKT and Bcl-xL expression in the pancreatic islets of rats were evaluated by Western blot methods.
Results
Blood glucose levels were significantly reduced in rats receiving asiatic acid after streptozocin administration. Asiatic acid concomitantly increased serum insulin levels in diabetic rats. Immunohistochemical staining revealed a marked preservation by asiatic acid of insulin-producing beta cells in the pancreatic islets of the diabetic rats. Furthermore, asiatic acid in vivo induced pro-survival Akt kinase activation and Bcl-xL expression in the pancreatic islets of diabetic rats.
Conclusions
These results suggest that asiatic acid exerts its glucose-lowering effects, in part through influences on beta-cell mass. Asiatic acid administration resulted in preservation and restoration of beta-cell mass and function in diabetic rodent models. Copyright © 2010 John Wiley & Sons, Ltd.
TL;DR: Fullerenol-pret treatment could protect tissues against CCl(4)-induced oxidative stress by improving the antioxidant ability, according to the pathological evaluation of Sprague-Dawley rats.
TL;DR: In the short term, the i.p. administration of AFS cells, is a safe procedure and allows their migration, homing and integration into various organs of healthy newborn rats.
Abstract: Despite being commonly used in clinical practice, the intraperitoneal (i.p.) route has been rarely used for cell delivery. We evaluated the capacity of amniotic fluid stem (AFS) cells, administered i.p., to diffuse systemically and to integrate into tissues of healthy newborn rats. AFS cells were obtained from pregnant GFP + Sprague–Dawley rats by c-kit selection. Wild-type Sprague–Dawley newborn rats were divided into two groups receiving i.p.: (1) 2 × 106 AFS cells (n = 12); (2) of phosphate buffer saline (PBS) (n = 2) at 24 and 48 h after birth. Animals were either killed at 96 h of life, and organs collected for gfp amplification, or at 3 weeks of life and tissues isolated for green fluorescence protein (GFP) immunofluorescence. No adverse effects were observed after i.p. injection of PBS or AFS cells. Gfp was amplified in at least one organ in all rats injected with AFS cells except one (11/12). The intestine was the organ found most frequently positive (67%) followed by liver (25%), spleen (16%), heart (16%), lungs (16%), femur (8%) and brain (0%). Immunohistochemistry confirmed PCR results. In the short term, the i.p. administration of AFS cells, is a safe procedure and allows their migration, homing and integration into various organs of healthy newborn rats.
TL;DR: It is concluded that in DN, oxidative stress initiates injuries to DRG neurons that finally results in death of neurons whereas administration of 25Mg-PMC16 by release of Mg and increasing ATP acts protectively.
Abstract: Diabetic neuropathy (DN) is a debilitating disorder occurring in most diabetic patients without a viable treatment yet. The present work examined the protective effect of 25Mg-PMC16 nanoparticle (porphyrin adducts of cyclohexil fullerene-C60) in a rat model of streptozotocin (STZ)-induced DN. 25Mg-PMC16 (0.5 lethal dose50 [LD50]) was administered intravenously in two consecutive days before intraperitoneal injection of STZ (45 mg/kg). 24Mg-PMC16 and MgCl2 were used as controls. Blood 2,3-diphosphoglycerate (2,3-DPG), oxidative stress biomarkers, adenosine triphosphate (ATP) level in dorsal root ganglion (DRG) neurons were determined as biomarkers of DN. Results indicated that 2,3-DPG and ATP decreased whereas oxidative stress increased by induction of DN which all were improved in 25Mg-PMC16-treated animals. No significant changes were observed by administration of 24Mg-PMC16 or MgCl2 in DN rats. It is concluded that in DN, oxidative stress initiates injuries to DRG neurons that finally results in death of neurons whereas administration of 25Mg-PMC16 by release of Mg and increasing ATP acts protectively.
TL;DR: The transport of MeHg-Cys complex was tissue-specific, and the increase in its uptake by liver and brain as well as a decrease in kidney was observed, and it was observed that mercury concentrations in brain and liver increased and renal Hg decreased, respectively.
Abstract: Methylmercury (MeHg) can cause deleterious effects in vertebrate tissues, particularly in the central nervous system. MeHg interacts with sulfhydryl groups from low and high molecular weight thiols in the blood, which can facilitate MeHg uptake into different tissues. The purpose of this study was to examine the effect of MeHg-Cysteine (MeHg-Cys) complex administration on Hg-uptake in cerebral areas (cortex and cerebellum), liver and kidney of adult mice. Animals were divided into four groups: control (1 mL/kg distilled water), MeHg (2 mg/kg), Cys (2 mg/kg) and MeHg-Cys complex (0.8 molar ratio). Mice received one intraperitoneal injection per day for 60 consecutive days. Treatment with MeHg significantly increased mercury concentrations in all tissues analysed when compared with the control group. The accumulation of mercury in brain and in liver was further increased in animals that received MeHg-Cys complex when compared with the MeHg alone group. However, renal Hg decreased in MeHg-Cys treated mice, when compared with the group treated only with MeHg. In summary, the transport of MeHg-Cys complex was tissue-specific, and we observed an increase in its uptake by liver and brain as well as a decrease in kidney.
TL;DR: Oleanolic acid isolated from the cuticular epithelium of Viscum articulatum Burm.
Abstract: Oleanolic acid is a molecule of current therapeutic interest. In the present study, oleanolic acid isolated from the cuticular epithelium of Viscum articulatum Burm. f. (Viscaceae) was investigated for its protective effects on gentamicin-induced renal damage in rats. Nephrotoxicity was induced in rats by intraperitoneal injection of gentamicin at a dose of 100 mg/kg/day for 8 days. The effect of Oleanolic acid administered orally at doses 40, 60 and 80 mg/kg/day was assessed biochemically by determination of albumin, urea and creatinine in serum and urine samples and also through histopathological examination of the kidneys. Oleanolic acid protected the rat kidneys from gentamicin-induced nephrotoxicity as evident from a decrease in the serum and urine levels of creatinine, albumin and urea. Oleanolic acid also protected the rat kidneys from histological alterations induced by gentamicin and also improved the glomerular filtration rate. Compared with an earlier report on intraperitoneal administration of oleanolic acid in paracetamol-induced nephrotoxicity in rats, the data show that orally administered oleanolic acid also exerted a nephroprotective effect even in the case of a nephrotoxicant such as gentamicin, which directly deteriorates the kidney function without prior metabolism.