17β-estradiol affects expression of nuclear factor-κB and tumor necrosis factor-α after focal cerebral ischemia reperfusion in rats
Wang Zhi-yong
Abstract
Wang Zhi-yong
Abstract
Objective To investigate the effects of 17β-estradiol(17β-E2) on the expression of nuclear factor kappaB(NF-κB) and tumor necrosis factor-α(TNF-α) after focal cerebral ischemia reperfusion.To study cerebral protection of mechanism 17β-E2.Methods Forty-nine female Wistar rats were randomly divided into 4 groups:group A ischemia/reperfusion(I/R)sham-operated;group B ovariectomy(OVX);group C:OVX+17β-E2;group D:sham-operated.Focal cerebral I/R was produced by right middle cerebral artery occlusion except for Group D.Group C rats were treated with 17β-E2(1 mg/kg) intraperitoneal injection for 7 days.NF-κBp65 and TNF-α were detected by immunohistochemistry.Brain tissues were stained with HE staining for observing the brain histopathological change.Results HE staining:compared with group A and group C,the damage of the brain tissue in group B was much heavier.Immunohistochemistry:in group B,the expressions of NF-κBp65 and TNF-α increased significantly after ischemia and reperfusion at the same time(P0.05).The expressions of NF-κBp65 and TNF-α at 24 h of all groups increased significantly compared with 2 h(P0.05).Conclusion Focal cerebral I/R induces significant increase in NF-κBp65 and TNF-α expression.17β-E2 can inhibit inflammatory reaction after cerebral ischemia by inhibiting the expressions of NF-κB and TNF-α.
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Objective To investigate the effects of 17β-estradiol(17β-E2) on the expression of nuclear factor kappaB(NF-κB) and tumor necrosis factor-α(TNF-α) after focal cerebral ischemia reperfusion.To study cerebral protection of mechanism 17β-E2.Methods Forty-nine female Wistar rats were randomly divided into 4 groups:group A ischemia/reperfusion(I/R)sham-operated;group B ovariectomy(OVX);group C:OVX+17β-E2;group D:sham-operated.Focal cerebral I/R was produced by right middle cerebral artery occlusion except for Group D.Group C rats were treated with 17β-E2(1 mg/kg) intraperitoneal injection for 7 days.NF-κBp65 and TNF-α were detected by immunohistochemistry.Brain tissues were stained with HE staining for observing the brain histopathological change.Results HE staining:compared with group A and group C,the damage of the brain tissue in group B was much heavier.Immunohistochemistry:in group B,the expressions of NF-κBp65 and TNF-α increased significantly after ischemia and reperfusion at the same time(P0.05).The expressions of NF-κBp65 and TNF-α at 24 h of all groups increased significantly compared with 2 h(P0.05).Conclusion Focal cerebral I/R induces significant increase in NF-κBp65 and TNF-α expression.17β-E2 can inhibit inflammatory reaction after cerebral ischemia by inhibiting the expressions of NF-κB and TNF-α.
Key concepts: Ischemia, Immunohistochemistry, Tumor necrosis factor alpha, Medicine, H&E stain, Necrosis, Group A, Internal medicine