Zhou Ziyi, Wang Lixian, Liao Ruhe, Chen Qin, Liu Changhui, Song Jianping, Deng Changsheng, Huang Xinan
Artemisinin Research Center, Guangzhou University of Chinese Medicine, Guangzhou 510405, China.
School of Pharmaceutical Sciences, Guangzhou University of Chinese Medicine, Guangzhou 510405, China.
Int J Mol Sci. 2025 Apr 24;26(9):4016. doi: 10.3390/ijms26094016.
This study investigated the protective effects of Garcinia biflavonoid 1 (GB1) against dextran sulfate sodium (DSS)-induced ulcerative colitis and its underlying mechanisms. Using wild-type (WT) and NLRP3 knockout (Nlrp3) mice, we demonstrated that GB1 administration significantly ameliorated colitis symptoms, as evidenced by improved body weight, disease activity index (DAI) scores, colon length, and histological damage in WT mice. Mechanistically, GB1 downregulated pro-inflammatory mediators (IL-6, NF-κB, and CD11b) while attenuating the expression of NLRP3 inflammasome components (ASC, Caspase-1, and IL-1β). Notably, these protective effects were abolished in Nlrp3 mice, confirming the essential role of NLRP3 in GB1-mediated mitigation of colitis. Furthermore, GB1 reinforced intestinal barrier integrity by preserving tight junctions, reducing permeability, and attenuating mucosal inflammation. Collectively, our findings highlight GB1 as a promising therapeutic candidate for colitis treatment, primarily through NLRP3 inflammasome suppression and intestinal barrier restoration.
本研究调查了藤黄双黄酮1（GB1）对葡聚糖硫酸钠（DSS）诱导的溃疡性结肠炎的保护作用及其潜在机制。使用野生型（WT）和NLRP3基因敲除（Nlrp3）小鼠，我们证明给予GB1可显著改善结肠炎症状，WT小鼠体重增加、疾病活动指数（DAI）评分改善、结肠长度增加以及组织学损伤减轻均证明了这一点。机制上，GB1下调促炎介质（IL-6、NF-κB和CD11b），同时减弱NLRP3炎性小体成分（ASC、半胱天冬酶-1和IL-1β）的表达。值得注意的是，这些保护作用在Nlrp3小鼠中被消除，证实了NLRP3在GB1介导的结肠炎缓解中的重要作用。此外，GB1通过维持紧密连接、降低通透性和减轻黏膜炎症来加强肠道屏障完整性。总的来说，我们的研究结果突出了GB1作为一种有前景的结肠炎治疗候选药物，主要是通过抑制NLRP3炎性小体和恢复肠道屏障。
