Angiopoietin-1 and Angiopoietin-2 Expression Imbalance Influence in Early Period After Subarachnoid Hemorrhage / 대한배뇨장애요실금학회지

PURPOSE: Microvascular endothelial integrity is important for maintaining the blood-brain barrier (BBB). However, subarachnoid hemorrhage (SAH) disrupts this integrity, making the BBB dysfunctional—an important pathophysiological change after SAH. Angiopoietin-1 (Ang-1) and angiopoietin-2 (Ang-2) regulate microvascular permeability by balancing each other’s expression. METHODS: This study investigated the dynamics of Ang-1 and Ang-2 expression after SAH and the protective effect of Ang-1 on BBB functioning using an endovascular puncture model of rat SAH. The Ang-1 and Ang-2 expression in brain tissue was determined by immunohistochemistry. In addition, Western blotting was used to estimate Ang-1 and Ang-2 concentration and to compare them at 6–72 hours post-SAH cortex and hippocampus. Evans blue viability assay was used to evaluate BBB permeability, and neurological testing was implemented to evaluate neurological impairment during SAH. RESULTS: It was found that following SAH, Ang-1 expression decreases and Ang-2 expression increases in the cortex, hippocampus, and microvessels. The Ang-1/Ang-2 ratio decreased as quickly as 6 hours after SAH and reached its lowest 1 day after SAH. Finally, it was found that exogenous Ang-1 reduces SAH-associated BBB leakage and improves neurological function in post-SAH rats. CONCLUSIONS: Our findings suggest that the equilibrium between Ang-1 and Ang-2 is broken in a period shortly after SAH, and the treatment of exogenous Ang-1 injection alleviates neurological dysfunctions through decreasing BBB destruction.

Roles of telomere and telomerase in the process of ginseno- side Rg1 protection against tert-butyl hydroperoxide-induced senescence in WI-38 cells / 中国药理学通报

Aim: To investigate the roles of telomere and telomerase in the process of ginsenoside Rg1 protection against tert-butylhydroperoxide (t-BHP)-induced senescence in WI-38 cells. Methods: Senile WI-38 cells were induced by t-BHP in vitro. Cell ultrastructure, cell cycle assay and β-galactosidase cytochemistry staining were used to evaluate cell senescence. Terminal restriction fragment (RTF) length and telomerase activity were delected by southern blotting and PCR-ELISA, respectively. Results: t-BHP induced cell senescence with characteristics of shortenned RTF length. Pretreatment with Rg1 significantly attenuated t-BHP-induced senescence in WI-38 cells. Compared with cells treated with t-BHP alone, Rg1 pretreatment markedly decreased the shortening of RTF length and resulted in telomerase activation. Conclusion: Activation of telomerase and prolonging of RTF length might be involved in the process of ginsenoside Rg1 protection against t-BHP-induced senescence in WI-38 cells.

Effect of ginsenoside Rg1 on expression of p21, cyclin E and CDK2 in the process of cell senescence / 药学学报

<p><b>AIM</b>To explore the possible role of p21, cyclin E and cyclin-dependent kinase 2 (CDK2) in the protection of ginsenoside Rg1 against tert-butylhydroperoxide (t-BHP)-induced senescence in WI-38 cells.</p><p><b>METHODS</b>The cellular ultrastructure, cytometric assay and beta-galactosidase (beta-gal) cytochemistry staining were used to evaluate cell senescence. The levels of of p21, cyclin E and CDK2 protein were detected by Western blot.</p><p><b>RESULTS</b>Pretreatment with Rg1 significantly attenuated t-BHP-induced senescence in WI-38 cells. Simultaneously, compared with cells treated with t-BHP alone, Rg1 pretreatment markedly decreased the level of p21 protein and increased the levels of CDK2 and cyclin E.</p><p><b>CONCLUSION</b>p21, cyclin E and CDK2 may be involved in the process of ginsenoside Rg1 protection against t-BHP-induced senescence in WI-38 cells.</p>