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Bilobalide protects against ischemia/reperfusion-induced oxidative stress and inflammatory responses via the MAPK/NF-?B pathways in rats.

ABSTRACT: BACKGROUND:Clinically, skeletal muscle ischemia/reperfusion injury is a life-threatening syndrome that is often caused by skeletal muscle damage and is characterized by oxidative stress and inflammatory responses. Bilobalide has been found to have antioxidative and anti-inflammatory effects. However, it is unclear whether bilobalide can protect skeletal muscle from ischemia/reperfusion injury. METHODS:The effects of bilobalide on ischemia/reperfusion-injured skeletal muscle were investigated by performing hematoxylin and eosin staining and assessing the wet weight/dry weight ratio of muscle tissue. Then, we measured lipid peroxidation, antioxidant activity and inflammatory cytokine levels. Moreover, Western blotting was conducted to examine the protein levels of MAPK/NF-?B pathway members. RESULTS:Bilobalide treatment could protected hind limb skeletal muscle from ischemia/reperfusion injury by alleviating oxidative stress and inflammatory responses via the MAPK/NF-?B pathways. CONCLUSIONS:Bilobalide may be a promising drug for I/R-injured muscle tissue. However, the specific mechanisms for the protective effects still need further study.

SUBMITTER: Li Y

PROVIDER: S-EPMC7350583 | biostudies-literature | 2020 Jul

REPOSITORIES: biostudies-literature

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Bilobalide protects against ischemia/reperfusion-induced oxidative stress and inflammatory responses via the MAPK/NF-휅B pathways in rats.

Li Ying Y Jiang Jiliang J Tong Liangcheng L Gao Tingting T Bai Lei L Xue Qing Q Xing Jianxin J Wang Qin Q Lyu Haoran H Cai Min M Sun Zhongyang Z

BMC musculoskeletal disorders 20200709 1

<h4>Background</h4>Clinically, skeletal muscle ischemia/reperfusion injury is a life-threatening syndrome that is often caused by skeletal muscle damage and is characterized by oxidative stress and inflammatory responses. Bilobalide has been found to have antioxidative and anti-inflammatory effects. However, it is unclear whether bilobalide can protect skeletal muscle from ischemia/reperfusion injury.<h4>Methods</h4>The effects of bilobalide on ischemia/reperfusion-injured skeletal muscle were i ...[more]

PMID: 32646398

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Project description:Background:Cerebral ischemia (CI) can lead to ischemic stroke. The most effective therapy for cerebral ischemic stroke is the early restoration of blood reperfusion. However, reperfusion after CI can result in cerebral ischemia reperfusion (CI/R) injury. This study aimed to detect the effect of eriocitrin on cerebral I/R injury and investigate the underlying mechanism. Methods:Seventy male Sprague-Dawley (SD) rats were randomly divided into 5 groups: the control group, the cerebral I/R group, the I/R + eriocitrin 8 mg/kg group, the I/R + eriocitrin 16 mg/kg group, and the I/R + eriocitrin 32 mg/kg group. Different doses of eriocitrin or 0.5% carboxymethyl cellulose sodium were administrated to the rats once daily for 7 days before middle cerebral artery occlusion (MCAO). PCR staining was performed to observe cerebral infarction. Hematoxylin and eosin (H&E) staining was carried out to observe the damage to the brain tissue. Terminal-deoxynucleotidyl transferase mediated nick end labeling (TUNEL) was used to detect apoptosis. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to detect the relative mRNA levels of related molecules. Western blot was used to detect the expression of related proteins. The detection kits were used to detect superoxide dismutase (SOD) and lactic dehydrogenase (LDH) activity, and malondialdehyde (MDA) content respectively. Enzyme-linked immunosorbent assay (ELISA) was used to detect TNF-radiation, interleukin-6 (IL-6), and interleukin-10 (IL-10). Results:The results showed that Eriocitrin significantly reduced the cerebral infarct volume, cerebral water content, and cerebral indexes. Eriocitrin treatment alleviated pathological injury, promoted cell proliferation, and inhibited cell apoptosis. Eriocitrin upregulated SOD activity and downregulated MDA and LDH content. Eriocitrin also effectively decreased the levels of IL-6 and tumor necrosis factor-? (TNF-?), but increased the content of IL-10 in serum and brain tissues. Furthermore, Eriocitrin increased the phosphorylation of nuclear factor erythroid 2-related factor (Nrf2), as well as the expressions of heme-oxygenase-1 (HO-1) and quinine oxidoreductase 1 (NQO1). Moreover, Eriocitrin decreased the phosphorylation of nuclear factor-?B (NF-?B) p65. Conclusions:Our results indicated that Eriocitrin attenuated oxidative injury and inflammatory response in rats with CI/R via the Nrf2/HO-1/NQO1/NF-?B signaling pathway.

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Dataset Information

Bilobalide protects against ischemia/reperfusion-induced oxidative stress and inflammatory responses via the MAPK/NF-?B pathways in rats.

Publications

Bilobalide protects against ischemia/reperfusion-induced oxidative stress and inflammatory responses via the MAPK/NF-휅B pathways in rats.

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