半夏泻心汤调控p53/SAT1/ALOX15通路干预胃癌前病变的研究OA
Study on Banxia Xiexin Decoction(半夏泻心汤)in intervening gastric precancerous lesions via regulating the p53/SAT1/ALOX15 pathway
目的 探讨半夏泻心汤调控大鼠胃组织p53/SAT1/ALOX15通路干预胃癌前病变的作用.方法 将24只SD大鼠随机分成空白组、模型组、半夏泻心汤组.空白组正常饲养,其他两组按照MNNG多因素复合法造模法.连续造模19周后,模型组和半夏泻心汤组继续自由饮用MNNG溶液,半夏泻心汤组在饮用MNNG基础上每日以半夏泻心汤1 mL/100 g剂量灌胃1次,连续干预10周.方法 HE染色观察光镜下胃黏膜病理组织学改变;RT-PCR检测p53、SAT1、ALOX15 mRNA表达水平;Western blot测定p53、SAT1、ALOX15蛋白表达水平.结果 模型组胃黏膜呈中-重度萎缩,部分可见异型增生,半夏泻心汤组胃黏膜呈轻度萎缩,且无异型增生.模型组大鼠p53、SAT1、ALOX15 mRNA表达较空白组降低(P<0.01),半夏泻心汤干预后p53、SAT1、ALOX 15 mRNA表达较模型组升高(P<0.01).模型组大鼠p53、SAT1、ALOX15蛋白较空白组降低(P<0.01),半夏泻心汤干预后p53、SAT1、ALOX15蛋白较模型组升高(P<0.01).结论 半夏泻心汤可能通过p53/SAT1/ALOX15通路,调控铁死亡,改善胃癌前病变大鼠模型病理状态.
Objective Expiloring the effect of Banxia Xiexin Decoction(半夏泻心汤,BXXXD)on regulating the p53/SAT1/ALOX15 pathway in rat gastic tissue and intervening in gastric precancerous lesions(GPL).Methods Twenty-four SD rats were randomly divided into a control group,a model group,and a BXXXD group.The control group received standard feeding,while the other two groups were modeled using the N-methyl-N'-nitro-N-nitrosoguanidine(MNNG)multi-factor composite method.After 19 weeks of continuous modeling,the model group and the BXXXD group continued to have free access to MNNG solution.Additionally,the BXXXD group received daily intragastric administration of BXXXD at a dose of 1 mL/100 g for 10 consecutive weeks.Gastric muco-sal histopathological changes were observed under light microscopy using HE staining.The mRNA expression levels of p53,SAT1,and ALOX15 were detected by RT-PCR.The protein expression levels of p53,SAT1,and ALOX15 were determined by Western blot(WB).Results HE staining revealed moderate to severe mucosal atrophy with some dysplasia in the model group,while the BXXXD group exhibited only mild atrophy and no dysplasia.Compared to the control group,the mRNA expression levels of p53,SAT1,and ALOX15 were significantly decreased in the model group(P<0.01).BXXXD intervention significantly increased the mRNA expres-sion levels of p53,SAT1,and ALOX15 compared to the model group(P<0.01).Similarly,the protein expression levels of p53,SAT1,and ALOX15 were significantly lower in the model group than in the control group(P<0.01),and these levels were higher after BXXXD intervention compared to the model group(P<0.01).Conclusion BXXXD may alleviate the pathological state of GPL in rats by regulating ferroptosis through the p53/SAT1/ALOX15 pathway.
马佳乐;王素盈;张馨元;高望;赵双梅;李慧臻
天津中医药大学第二附属医院,天津 300250天津中医药大学,天津 301617天津中医药大学,天津 301617天津中医药大学第二附属医院,天津 300250天津中医药大学第二附属医院,天津 300250天津中医药大学第二附属医院,天津 300250
医药卫生
半夏泻心汤胃癌前病变铁死亡p53精脒/精胺N1-乙酰基转移酶1花生四烯酸15-脂氧合酶
Banxia Xiexin Decoction(半夏泻心汤)Gastric precancerous lesionsFerroptosisp53Spermidine/spermine N1-acetyltransferase 1Arachidonate 15-lipoxygenase
《时珍国医国药》 2026 (10)
1807-1811,5
国家自然科学基金面上项目(82274442)天津市卫生健康委员会中医中西医结合科研课题(2023134)天津中医药大学第二附属医院育才计划(YC-FY202301)天津市教委科研计划项目(2024KJ043)
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