Intraperitoneal injection

About: Intraperitoneal injection is a research topic. Over the lifetime, 6550 publications have been published within this topic receiving 132023 citations. The topic is also known as: IP injection.

Gene and histomorphology alteration analysis in spermatogenesis arrest mouse model: a probable novel approach for infertility.

Abstract: Introduction Approximately 15% of couples in the reproductive age are struggling with infertility which, in nearly half of them, is caused by male factors. Material and methods The present study comprised of two groups of sixteen C57BL/6 mice; each mouse received either an intraperitoneal injection of 30 mg/kg of an alkylating agent or the same amount of distilled water. Testes were harvested 30 days following the injection. Morphometric analysis of hematoxylin and eosin (HE however, our investigations demonstrated that the azoospermia model could induce a 5-fold upregulation in Wilms Tumor-1 gene expression. Conclusions Development of an azoospermia model can upregulate Wilms Tumor-1 gene expression in a higher rate after 30 days; however, expression of the testis-specific genes, A-Kinase Anchoring Protein 4 and adenosine deaminase domain containing 1, decreased after the intervention. To the best of our knowledge, this upregulation could be related to spermatogenesis recovery after the follow-up period.

Interaction of Burn Toxin with Liver Cells and Artificial Lipid Bilayer Membranes

Abstract: Isolated murine skin was burnt in a standard high temperature burn model (250°C, 20 sec). From the burnt skin a lipid protein complex was isolated which exhibited toxic activities after intraperitoneal injection into acceptor mice [1]. Metabolic and ultrastructural studies using rat liver perfusion and isolated hepatocytes as target systems revealed alterations of cellular and especially of mitochondrial membranes and a reduced adaptability in gluconeogenesis and urea synthesis after stimulation with amino acids and lactate. After lipid extraction by organic solvents intravenous injection of the apo-protein into rabbits caused platelet aggregation and an increase of activity of lysosomal enzymes in serum.

Rats kidney morphological particularities and functions post-treatment with vernonia amygdalina extract and low-dose lead acetate

Abstract: This study was conducted to evaluate the effect of Vernonia amygdalina extract on Pb-induced kidney toxicity in Wistar rats. This investigation was carried out using 25 Wistar rat of both sexes, and the animals were divided into five groups: 5 rats per group. Group A served as the negative control group and was orally gavaged with 5mg/ kg body weight of normal saline daily. Group B served as the positive control and was treated with daily intraperitoneal (IP) injection of 8 mg/kg body weight of Pb acetate (Pb). Group C was treated with daily intraperitoneal (IP) injection of 8 mg/kg body weight of Pb along with 20 mg/kg body weight of Vernonia amygdalina extract orally. Group D was treated with daily intraperitoneal (IP) injection of 8 mg/kg body weight of Pb along with 40 mg/kg body weight of Vernonia amygdalina extract orally. Group 5 was treated with daily intraperitoneal (IP) injection of 8 mg/kg body weight of Pb along with 60 mg/kg body weight of Vernonia amygdalina extract orally. All treatments were done for a period of 28 days. The animals were sacrificed on the 29th day by cervical dislocation, then blood was collected by cardiac puncture, and kidneys were collected for histological profile. Lipid peroxidation (MDA), creatinine and urea level were all determined. There was marked elevation in MDA level with a concomitant depletion in urea and creatinine content in the group treated with only Pb when compared with the negative control group. There was a significant increase in proximal tubular area, distal tubular area, glomerular membrane thickness, area, perimeter and feret’s diameter and a significant decrease in proximal tubule, distal tubule ratio and cellularity in this group of rats when compared to the negative control. Oxidation and histological changes in the kidneys were successfully prevented by the pre- administration of Vernonia amygdalina as evidenced by creatinine and urea and MDA level. These were made evident as the morphological scores across all experimental groups were significantly different from those of the positive control (group 2). Based on the current findings, it can be concluded that Vernonia amygdalina successfully minimizes the deleterious effects in kidney function and histological coherence associated with nephrotoxicity by strengthening the antioxidant defense system, suppressing oxidative stress, and mitigating apoptosis.

[Sacubitril/valsartan attenuates left ventricular remodeling and improve cardiac function by upregulating apelin/APJ pathway in rats with heart failure].

Abstract: Objective: To investigate the effect and mechanism of sacubitril/valsartan on left ventricular remodeling and cardiac function in rats with heart failure. Methods: A total of 46 SPF-grade male Wistar rats weighed 300-350 g were acclimatized to the laboratory for 7 days. Rats were then divided into 4 groups: the heart failure group (n=12, intraperitoneal injection of adriamycin hydrochloride 2.5 mg/kg once a week for 6 consecutive weeks, establishing a model of heart failure); heart failure+sacubitril/valsartan group (treatment group, n=12, intragastric administration with sacubitril/valsartan 1 week before the first injection of adriamycin, at a dose of 60 mg·kg-1·d-1 for 7 weeks); heart failure+sacubitril/valsartan+APJ antagonist F13A group (F13A group, n=12, adriamycin and sacubitril/valsartan, intraperitoneal injection of 100 μg·kg-1·d-1 APJ antagonist F13A for 7 weeks) and control group (n=10, intraperitoneal injection of equal volume of normal saline). One week after the last injection of adriamycin or saline, transthoracic echocardiography was performed to detect the cardiac structure and function, and then the rats were executed, blood and left ventricular specimens were obtained for further analysis. Hematoxylin-eosin staining and Masson trichrome staining were performed to analyze the left ventricular pathological change and myocardial fibrosis. TUNEL staining was performed to detect cardiomyocyte apoptosis. mRNA expression of left ventricular myocardial apelin and APJ was detected by RT-qRCR. ELISA was performed to detect plasma apelin-12 concentration. The protein expression of left ventricular myocardial apelin and APJ was detected by Western blot. Results: Seven rats survived in the heart failure group, 10 in the treatment group, and 8 in the F13A group. Echocardiography showed that the left ventricular end-diastolic diameter (LVEDD) and the left ventricular end-systolic diameter (LVESD) were higher (both P<0.05), while the left ventricular ejection fraction (LVEF) and left ventricular fractional shortening (LVFS) were lower in the heart failure group than in the control group (both P<0.05). Compared with the heart failure group, rats in the treatment group were featured with lower LVEDD and LVESD (both P<0.05), higher LVEF and LVFS (both P<0.05), these beneficial effects were reversed in rats assigned to F13A group (all P<0.05 vs. treatment group). The results of HE staining showed that the cardiomyocytes of rats in the control group were arranged neatly and densely structured, the cardiomyocytes in the heart failure group were arranged in disorder, distorted and the gap between cells was increased, the cardiomyocytes in the treatment group were slightly neat and dense, and cardiomyocytes in the F13A group were featured similarly as the heart failure group. Masson staining showed that there were small amount of collagen fibers in the left ventricular myocardial interstitium of the control group, while left ventricular myocardial fibrosis was significantly increased, and collagen volume fraction (CVF) was significantly higher in the heart failure group than that of the control group (P<0.05). Compared with the heart failure group, the left ventricular myocardial fibrosis and the CVF were reduced in the treatment group (both P<0.05), these effects were reversed in the F13A group (all P<0.05 vs. treatment group). TUNEL staining showed that the apoptosis index (AI) of cardiomyocytes in rats was higher in the heart failure group compared with the control group (P<0.05), which was reduced in the treatment group (P<0.05 vs. heart failure group), this effect again was reversed in the F13A group (P<0.05 vs. treatment group). The results of RT-qPCR and Western blot showed that the mRNA and protein levels of apelin and APJ in left ventricular myocardial tissue of rats were downregulated in heart failure group (all P<0.05) compared with the control group. Compared with the heart failure group, the mRNA and protein levels of apelin and APJ were upregulated in the treatment group (all P<0.05), these effects were reversed in the F13A group (all P<0.05 vs. treatment group). ELISA test showed that the plasma apelin concentration of rats was lower in the heart failure group compared with the control group (P<0.05); compared with the heart failure group, the plasma apelin concentration of rats was higher in the treatment group (P<0.05), this effect was reversed in the F13A group (P<0.05 vs. treatment group). Conclusion: Sacubitril/valsartan can partially reverse left ventricular remodeling and improve cardiac function in rats with heart failure through modulating Apelin/APJ pathways.