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韩国红参调节帕金森病模型小鼠结肠的肠道紧密连接和炎症。

Korean Red Ginseng Regulates Intestinal Tight Junction and Inflammation in the Colon of a Parkinson's Disease Mouse Model.

机构信息

Department of Korean Medical Science, School of Korean Medicine; Yangsan, Korea.

Korean Medicine Research Center for Healthy Aging; Pusan National University, Yangsan, Korea.

出版信息

J Med Food. 2020 Dec;23(12):1231-1237. doi: 10.1089/jmf.2019.4640. Epub 2020 Oct 29.

DOI:10.1089/jmf.2019.4640
PMID:33121350
Abstract

Recent studies have determined that gastrointestinal function contributes to the control of Parkinson's disease (PD). Gastrointestinal dysfunction results in a leaky intestinal barrier, inducing inflammation in the gut. Korean red ginseng (KRG) is widely used for the treatment of numerous afflictions, including inflammation and neurodegenerative disease. We investigated changes in the intestinal tight junctions and proinflammatory cytokines in the colon, and alpha-synuclein (aSyn) in the colon and the substantia nigra (SN) of a PD mouse model. Eight-week-old male C57BL/6 mice were intraperitoneally administered 30 mg/kg of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) once a day for 5 days, and orally given 100 mg/kg of KRG for 12 consecutive days. Alterations in the levels of occludin, zonula occludens-1 (ZO-1), tumor necrosis factor-alpha (TNF-) and interleukin-1 beta (IL-1) in the colon, and the expressions of aSyn and tyrosine hydroxylase (TH) in the colon and the SN were evaluated. Oral administration of KRG significantly prevents the MPTP-induced motor dysfunction, and suppresses the MPTP-induced disruption of occludin and ZO-1, and suppresses the increase in TNF- and IL-1 in the colon of mice. In addition, KRG prevents accumulation of aSyn and TH in the colon and the SN. These results suggest that KRG has the potential to prevent MPTP-induced leaky gut barrier, inflammation, and accumulation of aSyn.

摘要

最近的研究表明,胃肠道功能有助于控制帕金森病(PD)。胃肠道功能障碍导致肠道屏障渗漏,引发肠道炎症。红参(KRG)被广泛用于治疗多种疾病,包括炎症和神经退行性疾病。我们研究了肠道紧密连接和结肠中促炎细胞因子以及α-突触核蛋白(aSyn)在结肠和黑质(SN)中的变化在 PD 小鼠模型中。将 8 周龄雄性 C57BL/6 小鼠腹腔内每天给予 30mg/kg 的 1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP)一次,连续 12 天每天口服 100mg/kg 的 KRG。评估了结肠中紧密连接蛋白、封闭蛋白-1(ZO-1)、肿瘤坏死因子-α(TNF-)和白细胞介素-1β(IL-1)的水平,以及结肠和 SN 中 aSyn 和酪氨酸羟化酶(TH)的表达变化。口服 KRG 可显著预防 MPTP 诱导的运动功能障碍,并抑制 MPTP 诱导的紧密连接蛋白和 ZO-1 的破坏,抑制 TNF-和 IL-1 在结肠中的增加。此外,KRG 可防止 aSyn 和 TH 在结肠和 SN 中的积累。这些结果表明,KRG 具有预防 MPTP 诱导的肠道渗漏、炎症和 aSyn 积累的潜力。

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