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作 者:邓媛[1] 方新华[1] 徐丽华 江萌[1] DENG Yuan;FANG Xinhua;XU Lihua;JIANG Yin(Hangzhou TCM Hospital Affiliated to Zhejiang Chinese Medical University,Hangzhou,Zhejiang 310007)
机构地区:[1]浙江中医药大学附属杭州市中医院,浙江杭州310007
出 处:《中国中医药科技》2024年第4期597-602,共6页Chinese Journal of Traditional Medical Science and Technology
基 金:浙江省中医药科技计划项目(2023ZF033)。
摘 要:目的:探究天沙合剂通过调节水通道蛋白(aquaporins,AQPs)对表皮生长因子受体抑制剂(epidermal growth factor receptor inhibitors,EGFRIs)造成的皮肤干燥的治疗作用机制。方法:将36只大鼠随机分为6组,分别为正常对照组、EGFRIs模型组、维生素E阳性对照组和低、中、高剂量天沙合剂组,每组6只。除正常对照组,其余5组大鼠通过连续28 d吉非替尼(37.5 mg/kg)灌胃给药构建EGFRIs诱导的背部皮肤干燥模型;从吉非替尼给药第15天开始,给予维生素E(13.5 mg/kg)或天沙合剂(8、4、2 mg/kg)干预,正常对照组和模型组给予等量生理盐水。给药结束后,观察背部皮疹情况,通过测量经皮失水评估皮肤损伤情况;通过HE染色评估皮肤组织病理变化;Western blot测定皮肤组织AQP1,AQP3和AQP5表达。结果:维生素E和高、中剂量天沙合剂组大鼠背部皮疹明显改善,经皮失水较模型组降低。维生素E和3剂量天沙合剂组大鼠皮肤组织病理变化减轻,皮肤组织AQP1、AQP3和AQP5表达增加。结论:天沙合剂可减轻EGFRIs诱导的皮肤损伤,改善其造成的皮肤病理变化,调节AQPs表达是其作用途径之一。Objective:To explore the mechanism of Tiansha Mixture on skin xerosis caused by EGFRIs by regulating aquaporins(AQPs).Methods:36 rats were divided into six groups:normal control,EGFRIs model,positive control,and low,medium,and high dose of Tiansha Mixture groups.All groups except for normal control group rats were Ig Gefitinib for 28 days to build EGFRIs-induced skin dryness model,vitamin E and Three dose of Tiansha Mixture groups were given the corresponding medicine(vitamin E13.5 mg/kg and Tiansha Mixture 8、4、2 mg/kg)for 14 days from the 15 th day Ig Gefitinib,normal control and EGFRIs model were given the same volume saline.Trans epidermal water loss(TEWL),HE staining were used to assess skin pathological damage;AQP1,AQP3,and AQP5,expressions of skin tissue were measured by Western blot.Results:Rats’skin rash of rats in vitamin E and high,medium dose Tiansha Mixture groups were significantly improved,TEWL level was reduced.Skin pathological damage of rats in vitamin E and three dose Tiansha Mixture groups were alleviated,AQP1,AQP3,AQP5 expressions of rats’skin tissue were increased.Conclusion:Tiansha Mixture can reduce EGFRIs-induced skin xerosis,improve skin tissue pathological injury,raising AQPs expressions was one of the mechanism.
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