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Abstract

Effects of Propofol Pretreatment on Microglial Pyroptosis in the Ischemic Penumbra of Rats Subjected to Cerebral Ischemia-Reperfusion

Author(s): Pengdan Ying, Shurong Liu, Yichuan Tian and Yang Cao*
Department of Anesthesiology, Children's Hospital, Zhejiang University School of Medicine, National Clinical Research Center for Child Health, Hangzhou, Zhejiang 310030, 1Medical imaging Research Institute of Longgang, The Third People's Hospital, Longgang, Shenzhen 518115, 2Department of Anesthesiology, Ningbo Fourth Hospital, Ningbo, Zhejiang 315470, China

Correspondence Address:
Yang Cao, Department of Anesthesiology, Ningbo Fourth Hospital, Ningbo, Zhejiang 315470, China, E-mail: 846576613@qq.com


To investigate the effect of propofol pretreatment on microglial pyroptosis in the ischemic penumbra of rats subjected to cerebral ischemia-reperfusion. 90 rats were randomly divided into Sham group, model group, nod-like receptor protein 3 inhibitor group, propofol low dose group and high dose group. Pathological changes in the hippocampal region of the ischemic penumbra of brain tissue were observed by hematoxylin and eosin staining; interleukin-1 beta and interleukin-18 levels were detected in the ischemic penumbra of cerebral tissue by enzyme-linked immunosorbent assay; immunofluorescence double staining was performed to detect the immunopositive co-expression of nod-like receptor protein 3, aspartate specific caspase 1 and ionized calcium adaptor protein 1 in the ischemic penumbra of cerebral tissue. Compared with the model group, the nod-like receptor protein 3 inhibitor group, propofol low dose group and propofol high dose group groups also had significantly lower neurological deficit scores, cerebral infarction volumes, and interleukin-1 beta and interleukin-18 levels, ionized calcium adaptor protein 1/nod-like receptor protein 3, ionized calcium adaptor protein 1/caspase 1 immunopositive co-expression, nod-like receptor protein 3, pro-caspase 1, P10, P20 and interleukin-1 beta protein expressions in the ischemic penumbra were significantly reduced (p<0.05), the pathological damage was improved to various degrees, and the number of nerve cells was increased. The neuroprotective effect of propofol pretreatment on cerebral ischemia-reperfusion injury may be related to the inhibition of microglial pyroptosis mediated by nod-like receptor protein 3 inflammasome.

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