Effects of Clematichinenoside AR on oxidative stress and inflammatory response regulation and nerve cell apoptosis in brain tissue of rats with cerebral ischemia reperfusion injury
Objective To study the effects of Clematichinenoside AR on oxidative stress response,nerve cell apoptosis,and inflammatory factors in the brain tissue of rats with cerebral ischemia reperfusion injury.Methods Forty-five rats were divided into control group,model group(rats with cerebral ischemia reperfusion injury),and Clematichinenoside AR low-(8 mg/kg),medium-(16 mg/kg),and high-(32 mg/kg)dose groups,with nine rats in each group.After 5 d of treatment,the rats were scored for neurological function.TTC staining was used to check cerebral infarction volume,TUNEL method to measure the degree of apoptosis,Western blot to determine the protein levels of cleaved-cysteine aspartic acid specific protease-3(C-Caspase-3),cleaved-cysteine aspartic acid specific protease-9(C-Caspase-9),and nuclear factor-κB p65(NF-κB p65)in the brain tissue,dinitrophenylhydrazine method to examine the lactate dehydrogenase(LDH)level,thiobarbituric acid method to measure the malondialdehyde(MDA)level,xanthine oxidation method to check the superoxide dismutase(SOD)level,colorimetry to examine the glutathione peroxidase(GSH-Px)level,and ELISA to determine the content of interleukin-1β(IL-1β)and tumor necrosis factor-α(TNF-α).Results Compared with the control group,the neurological function score in the model group increased(P<0.05),the cerebral infarction volume increased(P<0.05),the apoptosis index and the protein levels of C-Caspase-3 and C-Caspase-9 increased(P<0.05),the levels of LDH and MDA increased(P<0.05),SOD and GSH-Px levels decreased(P<0.05),the content of IL-1β and TNF-α increased(P<0.05),and the protein expression level of NF-κB p65 increased(P<0.05).Compared with the model group,the neurological function score in Clematichinenoside AR low-,medium-,and high-dose groups decreased successively(P<0.05),the cerebral infarction volume decreased successively(P<0.05),the apoptosis index and the protein levels of C-Caspase-3 and C-Caspase-9 decreased successively(P<0.05),the levels of LDH and MDA decreased successively(P<0.05),the levels of SOD and GSH-Px increased successively(P<0.05),the content of IL-1β and TNF-α decreased successively(P<0.05),and the protein expression level of NF-κB p65 decreased successively(P<0.05).Conclusion Clematichinenoside AR can reduce the level of oxidative stress response in brain tissue of rats with cerebral ischemia reperfusion injury,decrease the expressions of apoptosis factors of C-Caspase-3 and C-Caspase-9,and inhibit the release of inflammatory mediators,which may be related to downregulation of the NF-κB signaling pathway.
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