PDF(Pubmed)
Abstract：
Atherosclerosis (AS) is a common pathogenesis of cardiovascular diseases. Puerarin (Pue) is a Chinese herbal remedy used to prevent and treat AS. Here, this research investigated the effect of Pue on AS progression.
ApoE-/- mice were induced with acrolein. Body weight, blood lipid index, inflammatory factors, mitochondrial oxidative stress, and lipid deposition were detected. IL-6 and TNF-α were detected by ELISA. Oil red staining and H&E staining were used to observe the aortic sinus plaque lesions. Serum expressions of inflammatory factors IL-6, TNF-a, SOD, GSH and MDA were detected by ELISA, the mRNA expression levels of HDAC1 in the aorta were detected by RT-qPCR, and IL-6 and TNF-α in the aorta were detected by immunohistochemistry. JNK, p-JNK, OPA-1, and HDAC1 were detected by Western blotting.
Pue administration can effectively reduce lipid accumulation in AS mice induced by acrolein. Pue promoted the activity of SOD, GSH and MDA, and inhibited the formation of atherosclerotic plaques and the process of aortic histological changes. Pue reduced IL-6 and TNF-α. HDAC1 expression was down-regulated and p-JNK-1 and JNK protein expression was up-regulated.
Pue reduces inflammation and alleviates AS induced by acrolein by mediating the JNK pathway to inhibit HDAC1-mediated oxidative stress disorder.
ApoE-/- mice were induced with acrolein. Body weight, blood lipid index, inflammatory factors, mitochondrial oxidative stress, and lipid deposition were detected. IL-6 and TNF-α were detected by ELISA. Oil red staining and H&E staining were used to observe the aortic sinus plaque lesions. Serum expressions of inflammatory factors IL-6, TNF-a, SOD, GSH and MDA were detected by ELISA, the mRNA expression levels of HDAC1 in the aorta were detected by RT-qPCR, and IL-6 and TNF-α in the aorta were detected by immunohistochemistry. JNK, p-JNK, OPA-1, and HDAC1 were detected by Western blotting.
Pue administration can effectively reduce lipid accumulation in AS mice induced by acrolein. Pue promoted the activity of SOD, GSH and MDA, and inhibited the formation of atherosclerotic plaques and the process of aortic histological changes. Pue reduced IL-6 and TNF-α. HDAC1 expression was down-regulated and p-JNK-1 and JNK protein expression was up-regulated.
Pue reduces inflammation and alleviates AS induced by acrolein by mediating the JNK pathway to inhibit HDAC1-mediated oxidative stress disorder.
摘要：
目的：动脉粥样硬化（AS）是心血管疾病的常见发病机制。葛根素（Pue）是一种用于预防和治疗AS的中草药。这里,这项研究调查了Pue对AS进展的影响。
方法：用丙烯醛诱导ApoE-/-小鼠。体重,血脂指标,炎症因子，线粒体氧化应激，并检测到脂质沉积。ELISA法检测IL-6和TNF-α。采用油红染色和H&E染色观察主动脉窦斑块病变。血清炎症因子IL-6、TNF-α的表达,SOD,ELISA法检测GSH和MDA,RT-qPCR检测主动脉中HDAC1的mRNA表达水平,免疫组化法检测主动脉中IL-6和TNF-α的表达。JNK,p-JNK,通过蛋白质印迹法检测OPA-1和HDAC1。
结果：Pue给药可有效减少丙烯醛诱导的AS小鼠脂质蓄积。Pue促进了SOD的活性，GSH和MDA，并抑制动脉粥样硬化斑块的形成和主动脉组织学改变的过程。Pue降低IL-6和TNF-α。HDAC1表达下调,p-JNK-1和JNK蛋白表达上调。
结论：Pue通过介导JNK通路抑制HDAC1介导的氧化应激紊乱，减轻炎症和减轻丙烯醛诱导的AS。
方法：用丙烯醛诱导ApoE-/-小鼠。体重,血脂指标,炎症因子，线粒体氧化应激，并检测到脂质沉积。ELISA法检测IL-6和TNF-α。采用油红染色和H&E染色观察主动脉窦斑块病变。血清炎症因子IL-6、TNF-α的表达,SOD,ELISA法检测GSH和MDA,RT-qPCR检测主动脉中HDAC1的mRNA表达水平,免疫组化法检测主动脉中IL-6和TNF-α的表达。JNK,p-JNK,通过蛋白质印迹法检测OPA-1和HDAC1。
结果：Pue给药可有效减少丙烯醛诱导的AS小鼠脂质蓄积。Pue促进了SOD的活性，GSH和MDA，并抑制动脉粥样硬化斑块的形成和主动脉组织学改变的过程。Pue降低IL-6和TNF-α。HDAC1表达下调,p-JNK-1和JNK蛋白表达上调。
结论：Pue通过介导JNK通路抑制HDAC1介导的氧化应激紊乱，减轻炎症和减轻丙烯醛诱导的AS。
