Assay for lipid peroxides in animal tissues by thiobarbituric acid reaction

CA : A Cancer Journal for Clinicians

Definition: To what extent does the study allow us to draw conclusions about a causal effect between two or more constructs? Issues: Selection, maturation, history, mortality, testing, regression towrd the mean, selection by maturation, treatment by mortality, treatment by testing, measured treatment variables Increase: Eliminate the threats, above all do experimental manipulations, random assignment, and counterbalancing.

Reliability and validity

Yuming Yang,†,§ Qiang Zhao,‡,§ Wei Feng,† and Fuyou Li*,† †Department of Chemistry and State Key Laboratory of Molecular Engineering of Polymers and Institutes of Biomedical Sciences, Fudan University, Shanghai 200433, P. R. China ‡Key Laboratory for Organic Electronics and Information Displays (KLOEID) and Institute of Advanced Materials (IAM), Nanjing University of Posts and Telecommunications, Nanjing 210046, P. R. China.

Luminescent chemodosimeters for bioimaging.

Blood vessels are critical to deliver oxygen and nutrients to all of the tissues and organs throughout the body. The blood vessels that vascularize the central nervous system (CNS) possess unique properties, termed the blood-brain barrier, which allow these vessels to tightly regulate the movement of ions, molecules, and cells between the blood and the brain. This precise control of CNS homeostasis allows for proper neuronal function and also protects the neural tissue from toxins and pathogens, and alterations of these barrier properties are an important component of pathology and progression of different neurological diseases. The physiological barrier is coordinated by a series of physical, transport, and metabolic properties possessed by the endothelial cells (ECs) that form the walls of the blood vessels, and these properties are regulated by interactions with different vascular, immune, and neural cells. Understanding how these different cell populations interact to regulate the barrier properties is essential for understanding how the brain functions during health and disease.

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The Blood–Brain Barrier

Site-2 protease (S2P) is a membrane-embedded protease that site-specifically cleaves intramembrane transcription factors, a necessary step for their maturation. S2P is well known to regulate cholesterol biosynthesis and endoplasmic reticulum stress in mammalian cells. In this study, we hypothesized that S2P could be responsible for the regulation of cellular oxidative injury under oxidative stress. Wild type Chinese hamster ovary (WT CHO) cells and their mutant M19 cells with defective S2P gene were exposed to different oxidative stress conditions. Results showed that oxidative stress significantly up-regulated S2P expression in WT CHO cells. Notably, M19 cells had remarkably higher level of superoxide and elevated rates of cell death than WT CHO cells. The vulnerability to oxidative stress was reversed by the transfection of S2P gene but not rescued by exogenous supplement of cholesterol, oleate, and mevalonate, indicating that lack of S2P gene leads cells to be more vulnerable to oxidative stress. Furthermore, compared with WT CHO cells, M19 cells had higher nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activity and lower paraoxonase-2 expression. Taken together, these results suggest that S2P can be a protease responding to oxidative stress and has the function of regulating cellular oxidative injury.

/pdf/site-2-protease-responds-to-oxidative-stress-and-regulates-1h7zu7ih4l.pdf

Site-2 protease responds to oxidative stress and regulates oxidative injury in mammalian cells

Background Buyang Huanwu Decoction (BHD) is a classical Chinese Medicine formula empirically used for diabetic nephropathy (DN). However, its therapeutic efficacies and the underlying mechanisms remain obscure. In our study, we aim to evaluate the renoprotective effect of BHD on a streptozotocin (STZ)-induced diabetic nephropathy mouse model and explore the potential underlying mechanism in mouse mesangial cells (MCs) treated with high glucose in vitro, followed by screening the active compounds in BHD. Methods Mice were received 50 mg/kg streptozotocin (STZ) or citrate buffer intraperitoneally for 5 consecutive days. BHD was intragastrically administrated for 12 weeks starting from week 4 after the diabetes induction. The quality control and quantitative analysis of BHD were studied by high-performance liquid chromatography (HPLC). Renal function was evaluated by urinary albumin excretion (UAE) using ELISA. The mesangial matrix expansion and renal fibrosis were measured using periodic acid-schiff (PAS) staining and Masson Trichrome staining. Mouse mesangial cells (MCs) were employed to study molecular mechanisms. Results We found that the impaired renal function in diabetic nephropathy was significantly restored by BHD, as indicated by the decreased UAE without affecting the blood glucose level. Consistently, BHD markedly alleviated STZ-induced diabetic glomerulosclerosis and tubulointerstitial injury as shown by PAS staining, accompanied by a reduction of renal inflammation and fibrosis. Mechanistically, BHD inhibited the activation of TGF-β1/Smad3 and NF-κB signaling in diabetic nephropathy while suppressing Arkadia expression and restoring renal Smad7. We further found that calycosin-7-glucoside (CG) was one of the active compounds from BHD, which significantly suppressed high glucose-induced inflammation and fibrosis by inhibiting TGF-β1/Smad3 and NF-κB signaling pathways in mesangial cells. Conclusion BHD could attenuate renal fibrosis and inflammation in STZ-induced diabetic kidneys via inhibiting TGF-β1/Smad3 and NF-κB signaling while suppressing the Arkadia and restoring renal Smad7. CG could be one of the active compounds in BHD to suppress renal inflammation and fibrosis in diabetic nephropathy.

Buyang Huanwu Decoction protects against STZ-induced diabetic nephropathy by inhibiting TGF-β/Smad3 signaling-mediated renal fibrosis and inflammation.

Pinosylvin provides neuroprotection against cerebral ischemia and reperfusion injury through enhancing PINK1/Parkin mediated mitophagy and Nrf2 pathway

Recent progress suggests that neural stem/progenitor cells can potentially develop into new functional neurons in adult brain, offering hope for regeneration therapies for stroke treatment. Targeting adult neurogenesis becomes a novel and promising therapeutic strategy for brain repair and recovery of neurological functions. Traditional Chinese Medicine (TCM) has a long history with accumulated experiences and case reports using herbal formulas to treat stroke disability. The combination of Chinese herbal medicine and stem cell biology approaches provides great potential for post-stroke rehabilitations. In the last decade, large efforts have been made to investigate the molecular targets for the regulation of adult neurogenesis and to explore the active compounds and molecular targets of herbal medicine for regeneration therapy. Herein, we reviewed the current progress concerning the molecular targets and cellular signaling pathways involved in adult neurogenesis after cerebral ischemia. We then briefly introduced Chinese medical theory and herbs for stroke treatment in TCM. Finally, we reviewed the current knowledge about the effects of Chinese herbal formulas, active fractions and active compounds on promoting adult neurogenesis as well as their molecular targets. Although the precise mechanisms and molecular targets of herbal medicine for neurogenesis are still unclear, current progress at least provides a cue for exploring the therapeutic principles of Chinese herbal medicine and developing new drugs for brain repair after stroke.

/pdf/targeting-neurogenesis-a-promising-therapeutic-strategy-for-1pwgm566sz.pdf

Targeting Neurogenesis: A Promising Therapeutic Strategy for Post-Stroke Treatment with Chinese Herbal Medicine

The potential correlation of X-ray repair cross-complementing group 1 (XRCC1) Arg399Gln polymorphism with hepatocellular carcinoma (HCC) susceptibility is ambiguous. Taking account of inconsistent results of previous meta-analyses and new emerging literatures, we conducted a meta-analysis covering 15 case-control datasets to evaluate the relationship. Relevant studies from Medline, Embase and CNKI were retrieved. A fixedeffect model or a random-effect model, depending on between-study heterogeneity, were applied to estimate the association between XRCC1 polymorphism Arg399Gln and HCC risk with the results presented as odds ratios (ORs) and 95% confidence intervals (95% CIs). In accordance with Hardy-Weinberg equilibrium, 15 studies with data for 6,556 individuals were enrolled in this systematic review. For overall HCC,thr XRCC1 polymorphism Arg399Gln was significantly associated with HCC susceptibility in a homozygote model as well as in a dominant model (G/G vs. A/A, OR=1.253, p=0.028; G/G+A/G vs. A/A, OR= 1.281, p=0.047, respectively), but not in a heterozygote model (A/G vs. A/A, OR=1.271, p=0.066) or a recessive model (G/G vs. A/G + A/A, OR= 1.049, p=0.542). Similar results were also observed on stratification analysis by ethnicity (A/G vs. A/A, OR=1.357, p=0.025; G/G vs. A/A, OR=1.310, p=0.011; G/G+A/G vs. A/A, OR= 1.371, p=0.013). However, no potential contribution of XRCC1 Arg399Gln polymorphism to HCC susceptibility in HBV/HCV subgroups was identified. No publication bias was found in this study. In conclusion, the XRCC1 Arg399Gln polymorphism contributes to HCC susceptibility. Due to the lack of studies in Western countries, further large-sample and rigorous studies are needed to validate the findings.

http://koreascience.or.kr:80/article/JAKO201305981337680.pdf

Jiangang Shen

Papers

Site-2 protease responds to oxidative stress and regulates oxidative injury in mammalian cells

Buyang Huanwu Decoction protects against STZ-induced diabetic nephropathy by inhibiting TGF-β/Smad3 signaling-mediated renal fibrosis and inflammation.

Pinosylvin provides neuroprotection against cerebral ischemia and reperfusion injury through enhancing PINK1/Parkin mediated mitophagy and Nrf2 pathway

Targeting Neurogenesis: A Promising Therapeutic Strategy for Post-Stroke Treatment with Chinese Herbal Medicine

The XRCC1 Arg399Gln genetic polymorphism contributes to hepatocellular carcinoma susceptibility: an updated meta-analysis.