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首页> 外文期刊>Drug Design, Development and Therapy >Berberine Attenuates Arterial Plaque Formation in Atherosclerotic Rats with Damp-Heat Syndrome via Regulating Autophagy
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Berberine Attenuates Arterial Plaque Formation in Atherosclerotic Rats with Damp-Heat Syndrome via Regulating Autophagy

机译：Berberine通过调节自噬用湿热综合征在动脉粥样硬化大鼠中衰减动脉斑块形成

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Purpose: Berberine (BBR) is an effective component of Huanglian and has shown to attenuate atherosclerosis (AS); however, the detailed mechanism of BBR-mediated protective actions against AS remains elusive. This study was undertaken to examine the effects of BBR on aortic atherosclerotic plaque stability and the expression of autophagy-related proteins in AS rats with damp-heat syndrome or yang deficiency. Methods: Thirty SD rats were randomly divided into (1) control (CON); (2) damp-heat syndrome atherosclerosis (AS + DH); (3) yang deficiency syndrome atherosclerosis (AS + YX); (4) damp-heat syndrome atherosclerosis + BBR (AS + DH + BBR); (5) yang deficiency syndrome, atherosclerosis + BBR (AS + YX + BBR); and (6) damp-heat syndrome, atherosclerosis + BBR + 3-methyladenine (AS + DH + BBR + 3-MA) (n = 5/group) groups. Pathological morphology, macrophage plaque infiltration, inflammation, and LC3-II and P62 expression were assessed. Results: Compared with the CON group, the AS + DH and AS + YX groups had an increased plaque area in the aortic tissue with substantial foam cell and macrophage infiltration, and increased levels of IL-1β and TNF-α (P 0.01). After four weeks of BBR intervention, the plaque area in the AS + DH + BBR group was reduced with decreased foam cells and macrophage infiltration, and decreased levels of TNF-α and IL-1β, whereas LC3-II protein expression was increased and P62 protein expression was decreased in the AS + DH + BBR group when compared to AS + DH group. In addition, the AS + DH + BBR + 3-MA group exhibited a significantly enlarged plaque, substantial foam cell and macrophage infiltration, increased levels of IL-1β and TNF-α, and decreased LC3-II and P62 (P 0.01) expression when compared to the AS + DH + BBR group. Conclusion: Our results indicated that the BBR could inhibit arterial plaque formation and alleviate the inflammatory response in the aortic tissues in the AS rats with damp-heat syndrome possibly via promoting autophagy. The molecular mechanisms of BBR-mediated protective effects in this animal model still require further investigation.
机译：目的：小檗碱（BBR）是黄连的有效组成部分，并显示出衰减动脉粥样硬化（AS）;然而，BBR介导的保护行动仍然难以捉摸的详细机制。本研究旨在检测BBR对主动脉动脉粥样硬化斑块稳定性的影响及其在潮湿 - 热综合征或阳虚的大鼠中的自噬相关蛋白表达。方法：将30只SD大鼠随机分为（1）控制（CON）; （2）湿热综合征动脉粥样硬化（AS + DH）; （3）阳虚综合征动脉粥样硬化（AS + YX）; （4）湿热综合征动脉粥样硬化+ BBR（AS + DH + BBR）; （5）阳虚综合征，动脉粥样硬化+ BBR（AS + YX + BBR）; （6）湿热综合征，动脉粥样硬化+ BBR + 3-甲基腺嘌呤（AS + DH + BBR + 3- mA）（n = 5 /组）基团。评估病理形态，巨噬细胞斑块浸润，炎症和LC3-II和P62表达。结果：与CON组相比，AS + DH和AS + YX组在主动脉组织中具有大量泡沫细胞和巨噬细胞浸润的增加的斑块区域，以及增加IL-1β和TNF-α的水平（P <0.01） 。在BBR介入四周后，随着+ DH + BBR组的斑块区域随着泡沫细胞和巨噬细胞渗透而降低，并且降低TNF-α和IL-1β水平，而LC3-II蛋白表达增加，P62与As + DH组相比，AS + DH + BBR组中蛋白表达减少。此外，AS + DH + BBR + 3-MA组显示出显着扩大的斑块，大量泡沫细胞和巨噬细胞浸润，IL-1β和TNF-α的水平增加，降低LC3-II和P62（P <0.01）与AS + DH + BBR组相比的表达。结论：我们的研究结果表明，BBR可以通过促进自噬抑制随着潮湿综合征的大鼠主动脉组织中的动脉噬斑形成并减轻炎症反应。这种动物模型中BBR介导的保护作用的分子机制仍需要进一步调查。

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