Department of Gastroenterology, First Teaching Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin 300381, China.
2 National Clinical Research Center for Chinese Medicine Acupuncture and Moxibustion, Tianjin 300381, China.
J Tradit Chin Med. 2023 Feb;43(1):68-77. doi: 10.19852/j.cnki.jtcm.20220928.001.
: To investigate the efficacy of Qingchi San (青赤散,QCS), a preparation of Traditional Chinese Medicine, on ulcerative colitis (UC)in mice by inhibiting the nuclearfactor-kappa B (NF-κB) signaling pathway and nucleotide-binding oligomerization domain, leucine-rich repeat and pyrin domain-containing 3 (NLRP3) infla-mmasome formation.
: The UC model was established with male C57BL/6J as the animal model. Bodyweight, Disease Activity Index (DAI), colon length and weight were detected. Furthermore, colonic histology was performed by hematoxylin-eosin (HE) staining. interleukin-1β (IL-1β), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), myeloperoxidase (MPO) and superoxide dismutase (SOD) were performed by enzyme-linked immunosorbent assay. Cyclooxygenase 2 (COX2) and inducible nitric oxide synthase (iNOS) mRNA expression were conducted by real-time quantitative polymerase chain reaction (RT-qPCR). NF-κB, inhibitor of NF-κBα (iκBα), Phosphorylated inhibitor of NF-κBα (p-iκBα), caspase-1, NLRP3 and Apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC) protein expression were conducted by Western blotting.
: Compared with UC model group, Bodyweight was significantly increased in QCS treatment. At the same time, DAI was significantly decreased in QCS treatment. Colon length and weight and colonic histology were significantly improved in QCS treatment. Furth-ermore, the expression of IL-1β, IL-6, TNF-α, MPO, SOD, COX2, and iNOS were significantly decreased in QCS treatment. Finally, the expression of NF-κB signaling pathway-related proteins NF-κB, iκBα, p-iκBα, and the expression of NLRP3 inflammasome related proteins caspase-1, NLRP3 and ASC were significantly decreased in QCS treatment.
: Traditional Chinese drug QCS could treat UC by inhibiting the NF-κB signaling pathway and NLRP3 inflammasome formation in mice.
研究中药制剂青赤散（QCS）通过抑制核因子-κB（NF-κB）信号通路和核苷酸结合寡聚结构域、富含亮氨酸重复和吡咯烷域包含 3（NLRP3）炎症小体形成，对溃疡性结肠炎（UC）小鼠的疗效。
以雄性 C57BL/6J 为动物模型建立 UC 模型。检测体重、疾病活动指数（DAI）、结肠长度和重量。此外，通过苏木精-伊红（HE）染色进行结肠组织学检查。通过酶联免疫吸附试验（ELISA）检测白细胞介素-1β（IL-1β）、白细胞介素-6（IL-6）、肿瘤坏死因子-α（TNF-α）、髓过氧化物酶（MPO）和超氧化物歧化酶（SOD）。通过实时定量聚合酶链反应（RT-qPCR）检测环氧化酶 2（COX2）和诱导型一氧化氮合酶（iNOS）mRNA 表达。通过 Western blot 检测 NF-κB、NF-κBα 抑制剂（IκBα）、磷酸化 NF-κBα（p-IκBα）、半胱天冬酶-1、NLRP3 和含半胱天冬酶募集结构域的凋亡相关斑点样蛋白（ASC）蛋白表达。
与 UC 模型组相比，QCS 治疗组体重明显增加。同时，QCS 治疗组 DAI 明显降低。QCS 治疗组结肠长度和重量以及结肠组织学明显改善。此外，QCS 治疗组 IL-1β、IL-6、TNF-α、MPO、SOD、COX2 和 iNOS 的表达明显降低。最后，QCS 治疗组 NF-κB 信号通路相关蛋白 NF-κB、IκBα、p-IκBα 以及 NLRP3 炎症小体相关蛋白半胱天冬酶-1、NLRP3 和 ASC 的表达明显降低。
中药 QCS 可通过抑制 NF-κB 信号通路和 NLRP3 炎症小体在小鼠中的形成来治疗 UC。
