Ginsenoside Rg1 inhibits oxidative stress and inflammation in rats with spinal cord injury via Nrf2/HO-1 signaling pathway

神经保护 氧化应激 药理学 超氧化物歧化酶 丙二醛 脊髓 脊髓损伤 炎症 谷胱甘肽过氧化物酶 化学 医学 内科学 生物化学 精神科
作者
Zhen Zhang,Kejia Yang,Rui Mao,Donghai Zhong,Z. Xu,Jie Xu,Min Xiong
出处
期刊:Neuroreport [Ovid Technologies (Wolters Kluwer)]
卷期号:33 (2): 81-89 被引量:11
标识
DOI:10.1097/wnr.0000000000001757
摘要

In this study, our objective was to investigate the underlying mechanism of the neuroprotective role of ginsenoside Rg1 in attenuating spinal cord injury (SCI).A rat SCI model was established and treated with ginsenoside Rg1 and nuclear factor erythroid 2-related factor2(Nrf2) inhibitor all-trans retinoic acid (ATRA). The protective effects of ginsenoside Rg1 were evaluated by Basso, Beattie and Bresnahan (BBB) scale, hematoxylin/eosin staining, ELISA assay, western blotting and quantitative reverse transcription PCR (RT-qPCR).Ginsenoside Rg1 alleviated neuronal edema and bleeding in the injured spinal cord, reduced inflammatory cell infiltration and cell necrosis, further repaired the injured spinal cord structure, improved BBB motor score in the SCI rat model and improved hind limb motor function. Meanwhile, ginsenoside Rg1 significantly increased the content of antioxidant enzymes superoxide dismutase and glutathione, and inhibited the production of oxidative marker malondialdehyde. In addition, ginsenoside Rg1also significantly inhibits the activities of the inflammatory factors tumor necrosis factor-α, interleukin-1β (IL-1β) and interleukin-6 (IL-6) to reduce the inflammatory response after trauma. Furthermore, western blot and RT-qPCR also suggested that ginsenoside Rg1 could activate the protein expression of Nrf2 and heme oxygenase-1 (HO-1) after SCI, and the inhibition of ATRA on these improvements further verified the neuroprotective effect of Nrf2 and HO-1 in ginsenoside Rg1 on SCI.Ginsenoside Rg1 has a neuroprotective effect on SCI and can improve motor dysfunction caused by injury. The underlying mechanism may play antioxidative stress and anti-inflammatory effect by regulating the Nrf2/HO-1 signaling pathway.
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