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| Inhibiting MicroRNA-27b Regulation of Nrf2/ARE Signaling Pathway on Brain Injury in Rat Model of Hypertensive Cerebral Hemorrhage |
| LIU Xiaojiang, LI Jun, GUAN Yixiang |
| People's Hospital of Hai'an, Jiangsu Haian 226600, China |
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Abstract Objective: To investigate the effect of microrna-27b (mir-27b) inhibition on brain injury in hypertensive cerebral hemorrhage (HICH) rats, and to detect the expression of Nrf2 / are signal pathway and its downstream protein through the intervention of mir-27b antagonist, and to explore the therapeutic mechanism of mir-27b in anti-oxidation and neuroinflammation in hypertensive cerebral hemorrhage. Methods: The model of hypertensive intracerebral hemorrhage was established by injecting blood into the brain. QRT-PCR was used to detect the expression of mir-27b and Nrf2 mRNA in the brain of rats with hypertensive intracerebral hemorrhage; Western blot was used to detect the expression of Nrf2 / are signal pathway protein nuclear factor-related factor-2 (Nrf2), heme oxygenase (HO-1) and quinone oxidoreductase (NQO1) before and after administration of mir-27b antagonist; the kit was used to detect the superoxide dismutation of rats with hypertensive intracerebral hemorrhage before and after administration The changes of SOD, TNF - α and IL-1 β in rats with hypertensive cerebral hemorrhage were detected by TUNEL and flow cytometry. Results: Mir-27b and Nrf2 mRNA levels were significantly different before and after hich (P < 0.05); mir-27b antagonists could induce Nrf2, HO-1 and NQO1 protein expression in Nrf2 / are pathway; mir-27b antagonists could alleviate oxidative stress response (OS) in hich rats The mir-27b antagonist can alleviate the apoptosis of nerve cells and reduce the brain injury. Conclusion: Inhibition of mir-27b expression can significantly reduce the degree of brain injury in rats with hypertensive intracerebral hemorrhage, and its mechanism may be related to the activation of Nrf2 / are.
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2020, Vol. 26 
