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首页> 外文期刊>Journal of chemical neuroanatomy >SIRT1 activation by resveratrol reverses atrophy of apical dendrites of hippocampal CA1 pyramidal neurons and neurobehavioral impairments in moderate grade hepatic encephalopathy rats
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SIRT1 activation by resveratrol reverses atrophy of apical dendrites of hippocampal CA1 pyramidal neurons and neurobehavioral impairments in moderate grade hepatic encephalopathy rats

机译：白藜芦醇激活SIRT1逆转海马CA1金字塔神经元和中等肝脑脑病大鼠神经衰弱的萎缩

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摘要

A preliminary observation about resveratrol (RSV) dependent normalization of inflammatory and apoptotic factors in the cortex of hyperammonemic rat model of moderate grade hepatic encephalopathy (MoHE) led us to evaluate whether RSV is ultimately able to confer neuroprotection against MoHE pathogenesis and that it does so by activating its bonafide molecular target SIRT1. The present study compared the profile of relevant neurobehavioral pattern vs neuromorphometry of hippocampal CA1 neurons and SIRT1 activity in the hippocampus of the chronic liver failure (CLF) model of moderate grade HE (MoHE) rats induced by administration of 100 mg/kg body weight of thioacetamide i.p. for 10 days and in the CLF/MoHE rats treated with 10 mg/kg body weight RSV i.p. for 7 days. As compared to the control group rats, the MoHE rats showed significantly deranged pattern of memory and motor functions on MWM and rota rod tests, respectively. These behavioural deficits were associated with a significant reduction in apical dendrite length and number of branching points in the CA1 pyramidal neurons. Interestingly, all these parameters were found to be recovered back to their normal levels in the MoHE rats treated with RSV. Concordantly, MoHE associated declined SIRT1 activity in the hippocampus could be normalized back due to RSV treatment to those MoHE rats. Our findings suggest that RSV is able to normalize MoHE associated memory impairments and motor deficits vis a vis reversal of CA1 dendritic atrophy via SIRT1 activation.
机译：关于白藜芦醇（RSV）的初步观察（RSV）抑制炎症和凋亡因子的炎症和凋亡因子中的高级肝脑病（MOHE）的皮质凋亡因子导致我们评估RSV是否最终能够赋予MOHE发病机制的神经保护作用，并且它确实如此通过激活其Bonaidide分子靶SIRT1。本研究比较了通过施用100mg / kg体重诱导的中等肝炎大鼠的慢性肝功能衰竭（CLF）大鼠的海马相关神经兽性图案与海马CA1神经元和SIRT1活性的相关性神经形状的概况。硫代乙酰胺IP. 10天和在CLF / MOHE大鼠用10mg / kg体重RSV I.P处理。 7天。与对照组大鼠相比，MOHE大鼠分别显示出MWM和ROTA杆测试的显着的存储器和电动机功能模式。这些行为缺陷与Ca1金字塔神经元中的顶端树突长度和分支点数的显着降低有关。有趣的是，发现所有这些参数被发现回到用RSV处理的MoHe大鼠中的正常水平。一定，由于对那些Mohe大鼠的RSV治疗，Mohe相关的MoHe相关的患者在海马中的活力可以归一化。我们的研究结果表明，RSV能够通过SIRT1激活来规范MOHE相关的记忆障碍和电机缺陷。

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