Nrf2及其下游抗氧化因子在茶多酚防御UVB致無毛鼠皮膚急性光損傷中的表達及意義
發(fā)布時間:2018-03-10 20:25
本文選題:中波紫外線 切入點:茶多酚 出處:《中國皮膚性病學雜志》2017年08期 論文類型:期刊論文
【摘要】:目的探討Nrf2在茶多酚防御UVB致無毛鼠急性光損傷中的表達及意義。方法將10%茶多酚溶液均勻涂于BALB/C突變無毛鼠背部皮膚,30min后用約540m J/cm2UVB照射背部,連續(xù)3d,于第4天取皮膚組織備用檢測。采用光學顯微鏡觀察無毛鼠皮膚組織病理的變化情況,q-PCR檢測Nrf2 m RNA的表達量,免疫組化分析皮膚組織中Nrf2表達情況,ELISA法檢測Nrf2通路下游超氧化物歧化酶(SOD)、過氧化氫酶(CAT)、谷胱甘肽過氧化物酶(GSH-Px)的變化。結(jié)果外用10%茶多酚溶液可降低無毛鼠皮膚急性光損傷程度,免疫組化結(jié)果顯示茶多酚治療組Nrf2表達量明顯高于空白對照組及UVB照射組,Nrf2 m RNA的表達量及其該通路下游SOD,CAT,GSH-Px等抗氧化因子亦明顯增加(P0.05)。結(jié)論茶多酚能有效防御UVB致無毛鼠皮膚急性光損傷,與茶多酚激活Nrf2通路,啟動Nrf2及其Ⅱ相解毒酶基因表達,使得組織內(nèi)Nrf2通路下游抗氧化分子SOD,CAT,GSH-Px等濃度明顯增加直接相關(guān)。
[Abstract]:Objective to investigate the expression and significance of Nrf2 in the prevention of acute light injury induced by UVB in UVB rats. Methods 10% tea polyphenols solution was evenly applied to the dorsal skin of BALB/C mutant hairless mice for 30 minutes and irradiated with about 540m J / cm 2 UVB. After 3 consecutive days, the skin tissue was collected for the fourth day. The pathological changes of the skin tissue of hairless rats were observed by optical microscope. The expression of Nrf2 m RNA was detected by q-PCR. The expression of Nrf2 in skin tissue was analyzed by immunohistochemistry and Elisa was used to detect the changes of superoxide dismutase (SOD), catalase catalase (catalase) and glutathione peroxidase (GSH-Px) downstream of Nrf2 pathway. Results 10% tea polyphenol solution could reduce the skin of hairless rat skin. Skin acute light injury, The results of immunohistochemistry showed that the expression of Nrf2 in tea polyphenols treated group was significantly higher than that in blank control group and UVB irradiation group, and the expression of Nrf2 m RNA and antioxidant factors such as GSH-Px in the downstream of the pathway were also significantly increased. Conclusion Tea polyphenols can effectively defend UVB. Causing acute light damage to the skin of hairless mice, The activation of Nrf2 pathway by tea polyphenols, the activation of Nrf2 and the expression of detoxifying enzyme gene in phase 鈪,
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