scholarly journals Effect of matrine on JAK2/STAT3 signaling pathway and brain protection in rats with cerebral ischemia-reperfusion

2020 ◽  
Vol 29 (8) ◽  
pp. 959-966
Author(s):  
Jixing Chen ◽  
Cuiqin Huang ◽  
Lichao Ye ◽  
Boxin Yao ◽  
Meili Yang ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Signaling Pathway ◽  
Ischemia Reperfusion ◽  
Brain Protection ◽  
Stat3 Signaling ◽  
Cerebral Ischemia Reperfusion ◽  
Stat3 Signaling Pathway

Astragaloside IV Alleviates Cerebral Ischemia-Reperfusion Injury by Activating the Janus Kinase 2 and Signal Transducer and Activator of Transcription 3 Signaling Pathway

Pharmacology ◽  
2019 ◽  
Vol 105 (3-4) ◽  
pp. 181-189 ◽  
Author(s):  
ZhengHu Xu ◽  
Wei Liu ◽  
Huai Huang
Keyword(s):  
Cerebral Ischemia ◽  
Signaling Pathway ◽  
Ischemia Reperfusion ◽  
Janus Kinase ◽  
Signal Transducer ◽  
Astragaloside Iv ◽  
Stat3 Signaling ◽  
Cerebral Ischemia Reperfusion ◽  
Transcription 3

Astragaloside IV (AS-IV) is an active component extracted from the traditional Chinese herbal medicine. AS-IV is a neuroprotective component in cerebral ischemic models. However, roles of AS-IV in cerebral ischemia-reperfusion (I/R) injury and the underlying mechanisms are rarely investigated. The role of AS-IV in oxygen – glucose deprivation reoxygenation (OGD/R)-induced cell proliferation and apoptosis assays were analyzed by Cell Counting Kit-8 and Flow cytometric. Western Blot assays were performed to measure the related expression levels in SH-SY5Y cells. Meanwhile, activities of reactive oxygen species (ROS), superoxide dismutase (SOD), and malondialdehyde (MDA) in OGD/R-induced cells were determined by relative commercial kits. AS-IV was also used in cerebral I/R rat model, aimed to investigate the effects on cerebral infarct. The results indicated that OGD/R suppressed viability, enhanced apoptosis, which could be reversed by AS-IV treatment. Compared with the control group, the expression of p-JAK2 and p-STAT3 was significantly increased by AS-IV (60 μg/mL) under the OGD/R condition. Furthermore, AS-IV (60 μg/mL) treatment markedly increased SOD activity, whereas significantly decreased MDA activity and production of ROS in OGD/R-induced cells. The protective effects of AS-IV mentioned above were weaken or abolished while adding JAK2 inhibitor AG490. In addition, the effects of AS-IV on Janus kinase 2 and signal transducer and activator of transcription 3 (JAK2/STAT3) signaling in cerebral I/R injury were also verified in vivo. AS-IV protected against cerebral I/R injury and reversed by AG490. Therefore, in vitro and in vivo analyses suggested that AS-IV may protect against cerebral I/R injury partly mediated by JAK2/STAT3 signaling pathway and antioxidative effects. AS-IV may serve as a novel therapeutic regimen for cerebral I/R injury.

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