Article Publish Status: FREE
Abstract Title:

Ginsenoside Rb1 administration attenuates focal cerebral ischemic reperfusion injury through inhibition of HMGB1 and inflammation signals.

Abstract Source:

Exp Ther Med. 2018 Oct ;16(4):3020-3026. Epub 2018 Jul 26. PMID: 30214520

Abstract Author(s):

Anxin Liu, Weiwei Zhu, Lirui Sun, Guangming Han, Huiping Liu, Zhaoyu Chen, Li Zhuang, Wen Jiang, Xia Xue

Article Affiliation:

Anxin Liu


High-mobility group box 1 (HMGB1) is released after focal cerebral ischemia/reperfusion (I/R), and aggravates brain tissue damage. Ginsenoside Rb1 (Rb1), isolated from, has been reported to inhibit I/R-induced cell death in the brain. The present study aimed to investigate the protective ability of GRb1 on focal cerebral I/R rats and to explore its further mechanisms. A middle cerebral artery occlusion (MCAO) rat model was established and treated with different doses of Rb1. The neurological deficits were examined after reperfusion, and TTC staining was applied to assess the infarct volume. Histology and TUNEL staining were performed to evaluate pathological changes and neuronal cell apoptosis in brain tissues. HMGB1 and levels of inflammatory factors and proteins, were examined by ELISA or western blotting. Rb1 treatment notably improved the neurological deficits in an MCAO model, accompanied by decreased infarct volume in the brain tissues. Histological examination revealed that the necrotic tissue area in MCAO rats was also diminished by Rb1 treatment. Apoptosis induced by cerebral I/R was also attenuated by Rb1 treatment via downregulation of cleaved caspase-3 and caspase-9 levels. HMGB1 release was inhibited by Rb1 treatment in MCAO rats, and the levels of nuclear factor-κB, tumor necrosis factor-α, interleukin-6, inducible nitric oxide synthase and nitric oxide were also decreased. The present study suggests that Rb1 serves a protective role in I/R-induced cerebral-neuron injury, due to the decreased cerebral infarct volume of brain tissue. The mechanisms underlying these effects may be associated with the inhibition of HMGB1 inflammatory signals.

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