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Tenacissoside H promotes neurological recovery of cerebral ischaemia/reperfusion injury in mice by modulating inflammation and oxidative stress via TrkB pathway
Author(s) -
Zhang Rui,
Liu Cui,
Li Yang,
Chen Liang,
Xiang Jianfeng
Publication year - 2021
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/1440-1681.13398
Subject(s) - oxidative stress , tropomyosin receptor kinase b , nissl body , medicine , tunel assay , inflammation , neuroprotection , apoptosis , pharmacology , ischemia , tumor necrosis factor alpha , neurotrophic factors , anesthesia , endocrinology , receptor , pathology , chemistry , immunohistochemistry , staining , biochemistry
Cerebral ischaemia/reperfusion (I/R)‐induced acute brain injury remains a troublesome condition in clinical practice. The present study aimed to investigate the protective effect of tenacissoside H (TH) on I/R‐induced cerebral injury in mice. Here, a mouse model of middle cerebral artery occlusion (MCAO) was established by an improved Longa‐Zea method. TH was given by intraperitoneal injection once a day within 1 week before establishing the mouse MCAO model. The neurological functions of mice were evaluated and the apoptosis of neurons was also detected by the TUNEL method and Nissl's staining. ELISA and western blot were used to detect the expression of inflammatory factors, oxidation factors and proteins in the cerebral ischaemic cortex. The results revealed that TH dose‐dependently reduced neurological impairment, neuron apoptosis and brain oedema induced by MCAO. Furthermore, TH attenuated the expression of pro‐inflammatory cytokines (including interleukin (IL)‐1β, IL‐6 and tumour necrosis factor (TNF)‐α), iNOS and nuclear factor (NF)‐κB while increased production of anti‐inflammatory cytokines (IL‐4, IL‐10 and BDNF) and proteins of tropomyosin‐related kinase receptor B (TrkB) and PPARγ. Nevertheless, after the addition of TrkB inhibitor, the effects of TH above were mostly restrained. In conclusion, TH can protect mice against I/R‐induced neurological impairments via modulating inflammation and oxidative stress through TrkB signalling.