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Intervention effect of kushenol F on ulcerative colitis mice
- ZHONGGUO YAOFANG Vol. 35, Issue 4, Pages: 419-424(2024)
- 作者机构：
云南中医药大学中药学院， 昆明 650500
- 作者简介：
- 基金信息：
DOI：10.6039/j.issn.1001-0408.2024.04.07
CLC： R965Published：29 February 2024，
Received：03 August 2023，
Revised：14 December 2023，
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何旭东,倪皓雨,何金彪等.苦参醇F对溃疡性结肠炎小鼠的干预作用 Δ[J].中国药房,2024,35(04):419-424.
HE Xudong,NI Haoyu,HE Jinbiao,et al.Intervention effect of kushenol F on ulcerative colitis mice[J].ZHONGGUO YAOFANG,2024,35(04):419-424.
何旭东,倪皓雨,何金彪等.苦参醇F对溃疡性结肠炎小鼠的干预作用 Δ[J].中国药房,2024,35(04):419-424. DOI： 10.6039/j.issn.1001-0408.2024.04.07.
HE Xudong,NI Haoyu,HE Jinbiao,et al.Intervention effect of kushenol F on ulcerative colitis mice[J].ZHONGGUO YAOFANG,2024,35(04):419-424. DOI： 10.6039/j.issn.1001-0408.2024.04.07.
摘要
目的
2
探究苦参醇F（KSC-F）对溃疡性结肠炎（UC）小鼠的干预作用。
方法
2
将30只雄性C57BL/6J小鼠随机分为正常组、模型组、阳性对照组（柳氮磺吡啶，703 mg/kg）、KSC-F 50 mg/kg组（KSC-F50组）、KSC-F 100 mg/kg组（KSC-F100组），每组6只。除正常组外，其余各组小鼠均连续饮用3%葡聚糖硫酸钠水溶液7 d以复制UC模型；与此同时，各药物组灌胃相应药液，每天1次，连续10 d。实验期间，观察小鼠体重变化及排便情况，并于末次给药后进行疾病活动指数评分，观察其结肠组织病理形态，检测血清和结肠组织中炎症因子水平，以及结肠组织中炎症因子mRNA和炎症相关蛋白[白细胞介素1β（IL-1β）、叉头框蛋白O1（FOXO1）、磷脂酰肌醇3激酶（PI3K）、磷酸化PI3K（p-PI3K）、p38丝裂原激活的蛋白激酶（p38 MAPK）、磷酸化p38 MAPK（p-p38 MAPK）、磷酸化蛋白激酶B（p-Akt）等]的表达水平。
结果
2
KSC-F能缓解UC小鼠的体重减轻和结肠组织病变；可不同程度地降低血清中IL-1β、IL-6、IL-8、肿瘤坏死因子α（TNF-α）水平和结肠组织中IL-1β、IL-6、IL-17、TNF-α水平，升高血清和结肠组织中IL-10水平（
P
＜0.05或
P
＜0.01）；可不同程度地降低结肠组织中IL-1β、IL-17、TNF-α mRNA和p-PI3K、p-p38 MAPK、p-Akt蛋白的表达水平，提高结肠组织中IL-10 mRNA和FOXO1蛋白的表达水平（
P
＜0.05或
P
＜0.01）。
结论
2
KSC-F可通过抑制PI3K、Akt、p38 MAPK蛋白的激活，抑制IL-1β、IL-6、TNF-α等促炎因子的释放，促进抗炎因子IL-10的分泌，减轻结肠组织炎症损伤，从而改善UC小鼠的相关症状。
Abstract
OBJECTIVE
2
To investigate the intervention effect of kushenol F （KSC-F） on ulcerative colitis （UC） mice.
METHODS
2
Totally 30 male C57BL/6J mice were randomly divided into the normal group， model group， positive drug group （sulfasalazine， 703 mg/kg）， KSC-F 50 mg/kg group （KSC-F50 group）， and KSC-F 100 mg/kg group （KSC-F100 group）， with 6 mice in each group. Except for the normal group， the mice in the remaining groups were given 3% dextran sulfate sodium solution continuously for 7 days to induce UC model. Concurrently， administration groups received corresponding drug solution intragastrically， once a day， for 10 consecutive days. During the experiment， the changes in body weight and bowel movements of the mice were observed. Disease activity index scoring was performed after the last administration. The histopathological morphology of colonic tissue was examined. The levels of inflammatory factors in the serum and colon tissue were measured. Additionally， the mRNA expression of inflammatory factors， and the protein expressions of inflammation-related proteins [interleukin-1β （IL-1β）， forkhead box O1（FOXO1）， phosphoinositide 3-kinase（PI3K）， phosphorylated PI3K（p-PI3K）， p38 mitogen-activated protein kinase（p38 MAPK）， phosphorylated p38 MAPK（p-p38 MPAK） and phosphorylated protein kinase B（p-Akt）] were determined in colonic tissue.
RESULTS
2
KSC-F could alleviate weight loss and colonic tissue damage in UC mice. KSC-F reduced the levels of IL-1β， IL-6， IL-8 and tumor necrosis factor-α （TNF-α） in serum， as well as IL-1β， IL-6， IL-17 and TNF-α in colonic tissue to varying degrees and increased the levels of IL-10 in both serum and colonic tissue （
P
＜0.05 or
P
＜0.01）. Moreover， KSC-F decreased the expression levels of IL-1β， IL-17 and TNF-α mRNA， as well as p-PI3K， p-p38 MAPK， and p-Akt proteins in colonic tissue to varying degrees， and increased the expression levels of IL-10 mRNA and FOXO1 protein in colonic tissue （
P
＜0.05 or
P
＜0.01）.
CONCLUSIONS
2
KSC-F effectively alleviates UC symptoms in mice by inhibiting PI3K， Akt and p38 MAPK activation， mitigating the release of pro-inflammatory factors such as IL-1β， IL-6， TNF-α， promoting the anti-inflammatory factor IL-10 secretion， and reducing inflammation-induced colonic tissue damage.
关键词
苦参醇F溃疡性结肠炎炎症反应干预作用
Keywords
ulcerative colitisinflammatory reactionintervention effect
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