1. Academic Validation
  2. Gomisin J attenuates cerebral ischemia/reperfusion injury by inducing anti-apoptotic, anti-inflammatory, and antioxidant effects in rats

Gomisin J attenuates cerebral ischemia/reperfusion injury by inducing anti-apoptotic, anti-inflammatory, and antioxidant effects in rats

  • Bioengineered. 2022 Mar;13(3):6908-6918. doi: 10.1080/21655979.2022.2026709.
Xiaoli Min 1 2 Linping Zhao 3 Ying Shi 2 Jian Wang 2 Hongling Lv 2 Xiaoxiao Song 4 Qunyuan Zhao 5 Qing Zhao 1 Rui Jing 1 Jiayi Hu 1
Affiliations

Affiliations

  • 1 Department of Cerebrovascular Diseases, The Second Affiliated Hospital of Kunming Medical University, Kunming, Yunnan Province, China.
  • 2 Department of Internal Medicine, Clinical Medicine School, Yunnan Traditional Chinese Medicine University, Kunming, Yunnan Province, China.
  • 3 Yunnan Communications Vocational and Technical College, Institute of International Exchange, Kunming, Yunnan Province, China.
  • 4 Department of Epidemiology and Statistics, Public Health School, Kunming Medical University, Kunming, Yunnan Province, China.
  • 5 Department of Emergency, The Second Affiliated Hospital of Kunming Medical University, Kunming, Yunnan Province, China.
Abstract

Ischemic stroke is one of the leading causes of morbidity and mortality in humans. Cerebral ischemia-reperfusion (CIR) injury serves as a leading cause of stroke. Schisandra chinensis is a well-known Chinese traditional medicine. In this study, we explored the role of Gomisin J (GJ), a compound of S. chinensis, in CIR using a middle cerebral artery occlusion/reperfusion rat model and the possible mechanisms. We identified that GJ reduced neurological scores, cerebral infarction, and water content in the I/R rat brain. Importantly, GJ rescued I/R treatment-reduced neuron survival in the hippocampus, inhibited Apoptosis of ischemic tissues in I/R rats, increased B-cell lymphoma-extra-large (Bcl-xL) expression, and reduced the levels of cleaved Caspase-3, Bax, cyclooxygenase-2, nuclear factor kappa-B, and nitric oxide in I/R rat brain tissues. Furthermore, GJ treatment enhanced nuclear factor E2 related factor 2 (Nrf2) translocation, heme oxygenase-1 (HO-1) expression, superoxide dismutase and Glutathione Peroxidase activities, and glutathione level. Overall, GJ treatment GJ attenuates CIR injury by inducing anti-apoptotic, antioxidant, and anti-inflammatory effects in vivo.

Keywords

Cerebral ischemia-reperfusion injury; Gomisin J; apoptosis; inflammation; oxidative stress; stroke.

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