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[具体药物名称]对葡聚糖硫酸钠诱导的溃疡性结肠炎的治疗作用

Therapeutic Effects of against Ulcerative Colitis Induced by Dextran Sulfate Sodium.

作者信息

Kweon Do Yeong, Song Hee Jin, Kim Ji Eun, Jin You Jeong, Roh Yu Jeong, Seol Ayun, Park Ju Min, Lee Eun Suk, Choi Won Sik, Hwang Dae Youn

机构信息

Department of Bio-Industrial Machinery Engineering/Life, Industry Convergence Research Institute, College of Natural Resources and Life Science, Pusan National University, Miryang 50463, Republic of Korea.

Department of Biomaterials Science (BK21 FOUR Program)/Life, Industry Convergence Research Institute, Laboratory Animals Resources Center, College of Natural Resources and Life Science, Pusan National University, Miryang 50463, Republic of Korea.

出版信息

Curr Issues Mol Biol. 2023 Feb 9;45(2):1483-1499. doi: 10.3390/cimb45020096.

DOI:10.3390/cimb45020096
PMID:36826041
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9955819/
Abstract

() has been studied as a treatment option for ulcerative colitis (UC), but there is a lack of scientific evidence showing whether treatment with () can also be beneficial. To investigate the therapeutic potential of as a treatment for UC, clinical symptoms, histopathological characteristics of the colon, inflammatory response, and toxicity were analyzed in dextran sulfate sodium (DSS)-induced UC mice after administration of aqueous extracts of (AAS) for 7 days. The total polyphenol and tannin content of AAS was 272 µg/g and 163 µg/g, respectively. AAS exhibited significant antioxidant activity. Several clinical symptoms, including body weight, colon length, and hematochezia, remarkably improved in the DSS+AAS treated group compared to the DSS+Vehicle-treated group. In addition, similar improvements were detected in the histopathological characteristics and mucin-secreting ability in the colon of DSS-induced UC mice after the administration of AAS. The levels of infiltrated inflammatory cells and cytokine expression were significantly decreased in a dose-dependent manner in the colon of the DSS+AAS-treated group. These alterations in inflammatory response were accompanied by a significant recovery of the protein kinase C/extracellular signal-regulated kinase (PKC/ERK) and phosphatidylinositol-3-kinase/serine-threonine protein kinase (PI3K/Akt) signaling pathways. However, the levels of key markers for hepatotoxicity and nephrotoxicity consistently remained between those of the DSS+AAS-treated and the No groups. Therefore, the results of the present study provide novel evidence that AAS may improve the clinical symptoms and attenuate the inflammatory response in DSS-induced UC mice and does not have any significant hepatotoxicity or nephrotoxicity.

摘要

()已被作为溃疡性结肠炎(UC)的一种治疗选择进行研究,但缺乏科学证据表明用()治疗是否也有益。为了研究()作为UC治疗方法的治疗潜力,在给予()水提取物(AAS)7天后,对葡聚糖硫酸钠(DSS)诱导的UC小鼠的临床症状、结肠组织病理学特征、炎症反应和毒性进行了分析。AAS的总多酚和单宁含量分别为272μg/g和163μg/g。AAS表现出显著的抗氧化活性。与DSS+赋形剂处理组相比,DSS+AAS处理组的几种临床症状,包括体重、结肠长度和便血,有显著改善。此外,在给予AAS后,DSS诱导的UC小鼠结肠的组织病理学特征和粘蛋白分泌能力也有类似改善。DSS+AAS处理组结肠中浸润的炎症细胞水平和细胞因子表达以剂量依赖性方式显著降低。炎症反应的这些改变伴随着蛋白激酶C/细胞外信号调节激酶(PKC/ERK)和磷脂酰肌醇-3-激酶/丝氨酸-苏氨酸蛋白激酶(PI3K/Akt)信号通路的显著恢复。然而,肝毒性和肾毒性关键标志物的水平始终介于DSS+AAS处理组和未处理组之间。因此,本研究结果提供了新的证据,表明AAS可能改善DSS诱导的UC小鼠的临床症状并减轻炎症反应,且没有任何显著的肝毒性或肾毒性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7c76/9955819/f650fdc10537/cimb-45-00096-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7c76/9955819/72f98ed65e6c/cimb-45-00096-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7c76/9955819/48ac0f007352/cimb-45-00096-g002a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7c76/9955819/6b978f702e5e/cimb-45-00096-g003a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7c76/9955819/e036ea2b0b34/cimb-45-00096-g004a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7c76/9955819/34da4fcb8539/cimb-45-00096-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7c76/9955819/f650fdc10537/cimb-45-00096-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7c76/9955819/72f98ed65e6c/cimb-45-00096-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7c76/9955819/48ac0f007352/cimb-45-00096-g002a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7c76/9955819/6b978f702e5e/cimb-45-00096-g003a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7c76/9955819/e036ea2b0b34/cimb-45-00096-g004a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7c76/9955819/34da4fcb8539/cimb-45-00096-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7c76/9955819/f650fdc10537/cimb-45-00096-g006.jpg

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