Effects of butylphthalide on oxidative stress inflammatory pathway of cerebral ischemia-reperfusion injury in rats
- Author:
You HUANG
1
Author Information
- Publication Type:Journal Article
- Keywords: Butylphthalide; Cerebral ischemia-reperfusion injury; HO-1; Nrf2; Oxidative stress
- From: Journal of Xi'an Jiaotong University(Medical Sciences) 2020;41(2):201-205
- CountryChina
- Language:Chinese
- Abstract: Objective: To observe the effects of butylphthalide on cerebral ischemia-reperfusion injury in rats. Methods: We divided 90 SD rats into sham-operation group, model group, low-dose butylphthalide group, medium-dose butylphthalide group, high-dose butylphthalide group, and ATRA group. Neurological impairment score (NDS) was used to evaluate neurological function. TTC staining was used to calculate the volume of ischemic brain tissue. The xanthine oxidase method was used to detect SOD. The thiobarbituric acid colorimetry was used to detect MDA. ELISA was used to detect IL-6 and TNF-α expressions. The Real-time PCR was used to detect HO-1 gene expression. Western blot was used to detect Nrf2 and HO-1 protein expressions. Results: In low-, medium-, and high-butylphthalide groups, the NDS; volume of ischemic brain tissue; expressions of MDA, IL-6 and TNF-α; 2-△△Ct value of HO-1; protein expressions of Nrf2 and HO-1 were lower than those in model group (P<0.05), but SOD expression was higher than that in model group (P<0.05). The NDS; volume of ischemic brain tissue; expressions of MDA, IL-6 and TNF-α; 2-△△Ct value of HO-1; protein expressions of Nrf2 and HO-1 decreased in a dose-depended manner in low-, medium-, and high-butylphthalide groups, and SOD expression was increased in a dose-depended manner (P<0.05). Conclusion: Butylphthalide can play an antioxidant role by up-regulating Nrf2/HO-1 pathway, which benefits neuroprotective function in cerebral ischemia-reperfusion rats.
