1. Academic Validation
  2. Tenacissoside H promotes neurological recovery of cerebral ischaemia/reperfusion injury in mice by modulating inflammation and oxidative stress via TrkB pathway

Tenacissoside H promotes neurological recovery of cerebral ischaemia/reperfusion injury in mice by modulating inflammation and oxidative stress via TrkB pathway

  • Clin Exp Pharmacol Physiol. 2021 May;48(5):757-769. doi: 10.1111/1440-1681.13398.
Rui Zhang 1 Cui Liu 2 Yang Li 1 Liang Chen 3 Jianfeng Xiang 3
Affiliations

Affiliations

  • 1 Department of NICU, Affiliated Hospital of Qingdao University, Qingdao, China.
  • 2 Department of Cardiovascular Surgery, Affiliated Hospital of Qingdao University, Qingdao, China.
  • 3 Interventional Department, Shanghai Jiao Tong University Affiliated Sixth People's Hospital South Campus (Shanghai Fengxian District Central Hospital), Shanghai, China.
Abstract

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.

Keywords

TrkB; inflammatory response; ischaemia/reperfusion injury; tenacissoside H.

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