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Anti-apoptotic mechanisms of lyophilized powder of catapol and puerarin against brain ischemia damage on neurovascular unit cells
Author(s): XUE Qiang, WANG Hong-yu, SUN Wen-wei, YANG Sheng, WEI Shu-yong, XU Xiao-yu, College of Pharmaceutical Sciences·College of Chinese Medicine, Southwest University, Rongchang Campus of Southwest University, Institute of Chinese Medicine, Southwest University, Chongqing Engineering Research Center for Pharmacological Evaluation
Pages: 1716-
1722
Year: 2016
Issue:
5
Journal: China Journal of Traditional Chinese Medicine and Pharmacy
Keyword: Lyophilized powder of catalpol and puerarin; Neurovascular unit; Ischemic stroke; Oxygen and glucose deprivation; Neuroprotection; Apoptosis;
Abstract: Objective: To observe the anti-apoptotic mechanisms of lyophilized powder of catalpol and puerarin(C-P) against brain ischemia damage on neurovascular unit cells. Methods: In ischemic/reperfusion(I/R) rats and in oxygen and glucose deprivation/reperfusion(OGD/R) damaged NVU models, the anti-apoptotic mechanisms of C-P against brain ischemia damage on neurovascular unit cells was investigated. Results: In I/R rats, the C-P at all of the doses(49.0, 24.5, 12.25μg/m L) significantly inhibited the expression of Cleaved caspase-3, Caspase-3 and Bax(P<0.01, P<0.05), and decreased the apoptosis rates of neurons, brain microvascular endothelial cells(BMECs) and astrocytes in ischemic regions(P<0.01). It also significantly reduced the infarct volume(P<0.01), and ameliorated neurological deficiency in I/R rats(P<0.01). Further, in OGD/R-damaged NVU, 49μg/m L C-P have same effect on inhibiting the expression of Cleaved caspase-3, Caspase-3 and Bax(P<0.01), and decreasing the apoptosis rates of the three types of cells(P<0.01). Additionally, it significantly increased the neuronal axon length, and the number of astrocytes and BMECs(P<0.01). Conclusion: The C-P could protect NVU cells from brain ischemia damage through inhibiting the apoptosis of neurons, BMECs and astrocytes simultaneously, thus ameliorating the neurological deficiency of I/R rats with the decreasing of cerebral infarct volume.
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