Let-7a gene knockdown protects against cerebral ischemia/reperfusion injury

来源 :Neural Regeneration Research | 被引量 : 0次 | 上传用户:liutingkaoyanhao
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The micro RNA(mi RNA) let-7 was one of the first mi RNAs to be discovered, and is highly conserved and widely expressed among species. let-7 expression increases in brain tissue after cerebral ischemia/reperfusion injury; however, no studies have reported let-7 effects on nerve injury after cerebral ischemia/reperfusion injury. To investigate the effects of let-7 gene knockdown on cerebral ischemia/reperfusion injury, we established a rat model of cerebral ischemia/reperfusion injury. Quantitative reverse transcription-polymerase chain reaction demonstrated that 12 hours after cerebral ischemia/reperfusion injury, let-7 expression was up-regulated, peaked at 24 hours, and was still higher than that in control rats after 72 hours. Let-7 gene knockdown in rats suppressed microglial activation and inflammatory factor release, reduced neuronal apoptosis and infarct volume in brain tissue after cerebral ischemia/reperfusion injury. Western blot assays and luciferase assays revealed that mitogen-activated protein kinase phosphatase-1(MKP1) is a direct target of let-7. Let-7 enhanced phosphorylated p38 mitogen-activated protein kinase(MAPK) and c-Jun N-terminal kinase(JNK) expression by down-regulating MKP1. These findings suggest that knockdown of let-7 inhibited the activation of p38 MAPK and JNK signaling pathways by up-regulating MKP1 expression, reduced apoptosis and the inflammatory reaction, and exerted a neuroprotective effect following cerebral ischemia/reperfusion injury. The micro RNA (mi RNA) let-7 was one of the first mi RNAs to be discovered, and is highly conserved and widely expressed among species. Let-7 expression increases in brain tissue after cerebral ischemia / reperfusion injury; however, no studies has investigated the effects of let-7 gene on nerve injury after cerebral ischemia / reperfusion injury. we established a rat model of cerebral ischemia / reperfusion injury. Quantitative reverse transcription-polymerase chain reaction prototype that up-regulated, peak-at-24 hours, and was still more than that in control rats after 72 hours. Let-7 gene knockdown in rats suppressed microglial activation and inflammatory factor release, reduced neuronal apoptosis and infarct volume in brain tissue after cerebral ischemia / reperfusion injury. Western blot assays and luciferase assays revealed that mit Let-7 enhanced phosphorylated p38 mitogen-activated protein kinase (MAPK) and c-Jun N-terminal kinase (JNK) expression by down-regulating MKP1. These findings suggest that knockdown of let-7 inhibited the activation of p38 MAPK and JNK signaling pathways by up-regulating MKP1 expression, reduced apoptosis and the inflammatory reaction, and exerted a neuroprotective effect following cerebral ischemia / reperfusion injury.
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