Mitochondrial oxidative stress in vascular endothelial cell and atherosclerosis / 药学实践杂志

The injury of vascular endothelial cell function is the beginning of the pathological process of atherosclerosis. Mitochondrial oxidative stress is closely related to vascular endothelial cell function, which causes the dysfunction of vascular endothelial cell by inducing mitophagy, reducing nitric oxide production, inflammation, cellular metabolic imbalance and apoptosis. Meanwhile, vascular endothelial cell could also maintain their homeostasis by regulating mitochondrial oxidative stress. The molecular signaling pathways of the vascular endothelial cell injury caused by mitochondrial oxidative stress in the pathological process of atherosclerosis were outlined in this review, which provided reference for further research on the molecular mechanism between mitochondrial oxidative stress and endothelial damage.

Piperazine derivate ofβ-elemene(DX2) induces human hepatoma HepG2 cell apoptosis through mitochondrial pathway / 国际药学研究杂志

Objective To study the antiproliferative effect of DX2, a piperazine derivate of β-elemene, on human hepatoma HepG2 cells. Methods Cell viability was measured by MTT method. Morphological changes were observed by phase contrast microscopy and acridine orange staining. Apoptotic cell ratio was measured by flow cytometric analysis. Protein level was detected by Western blot analysis. Results DX2 Induced apoptotic morphological changes in HepG2 cells and increased the ratio of apoptotic cells. Treatment of HepG2 cells with DX2 increased the Bax/Bcl-2 ratio, induced the activation of caspase-9 and caspase-3 and caused the degradation of ICAD which was the substrate of capase-3. Conclusion DX2 Induces HepG2 cell death via activation of intrinsic mitochondrial pathway.

Role of gonadotropin-releasing hormone on advancing rat puberty onset induced by estradiol / 中国药理学与毒理学杂志

OBJECTIVE To investigate the role of gonadotropin-releasing hormone (GnRH) in es-tradiol(E2 ) induced advance of puberty onset in rats. METHODS Postnatal day 18 SD rats were given a daily intragastric administration of corn oil or E2(50 μg.kg-1 ) for consecutive 5 d. The day of vaginal opening (VO), pathological changes in ovary and protein expression levels of GnRH, G protein-coupled receptor 54 ( GPR54) and phospholipase C ( PLC) in hypothalamus were observed. RESULTS As compared to corn oil controll group, VO was advanced by about 12.2 d, corpus luteum was observed in the ovary section, and the protein expression levels of GnRH,GPR54 and PLC in hypothalamus were significantly increased by 47%, 55% and 56% in E2 group, respectively. CONCLUSION E2 induced onset of puberty advance may be closely related to regulation of the expression of GnRH, GPR54 and PLC in hypothalamus.