炎症性肠病(IBD)是一种全球性的慢性炎症性疾病,通常需要终身护理。迄今为止,仍然迫切需要发现针对这种疾病的新型抗炎治疗剂。生脉散(SMS)是一种具有治疗气阴两虚证的传统中药处方,最近的研究表明,SMS具有抗炎潜力。然而,SMS对胃肠系统的影响仍然缺乏研究,其在IBD中的治疗潜力和潜在的分子机制尚未被发现。在这项研究中,我们检查了SMS在IBD中的治疗功效及其抗炎活性和潜在的分子机制,体内和体外。
在DSS诱导的急性结肠炎小鼠模型中评估SMS在IBD中的治疗功效。体重,大便稠度,直肠出血,结肠长度,器官系数,结肠组织中的细胞因子水平,免疫细胞浸润,和结肠病理学进行评估。通过评估促炎细胞因子分泌和NF-κB,进一步检查了SMS在脂多糖(LPS)诱导的巨噬细胞中的抗炎活性和相关分子机制。MAPK,STAT3和NLRP3信令。
■SMS显着改善了急性结肠炎小鼠的疾病严重程度,正如疾病活动指数的改善所证明的那样,结肠形态学,和组织学损伤。此外,SMS减少了促炎细胞因子的产生和结肠组织中免疫细胞的浸润。此外,在LPS诱导的巨噬细胞中,我们证明SMS显著抑制细胞因子的产生并抑制多种促炎信号通路的激活,包括NF-κB,MAPK,和STAT3。SMS还消除了NLRP3炎性体激活,并抑制了随后的caspase-1激活和IL-1β分泌,为IBD的治疗提供了新的治疗靶点。这些机理发现也在体内测定中得到证实。
■本研究介绍了SMS的抗炎活性和详细的分子机制,在体外和体内。重要的是,我们首次强调SMS作为IBD有效治疗剂的潜力.
UNASSIGNED: Inflammatory bowel disease (IBD) is a globally emergent chronic inflammatory disease which commonly requires lifelong care. To date, there remains a pressing need for the discovery of novel anti-inflammatory therapeutic agents against this disease. Sheng Mai San (SMS) is a traditional Chinese medicine prescription with a long history of use for treating Qi and Yin deficiency and recent studies have shown that SMS exhibits anti-inflammatory potential. However, the effects of SMS on the gastrointestinal system remain poorly studied, and its therapeutic potential and underlying molecular mechanisms in IBD have yet to be discovered. In this study, we examined the therapeutic efficacy of SMS in IBD and its anti-inflammatory activity and underlying molecular mechanism, in vivo and in vitro.
UNASSIGNED: The therapeutic efficacy of SMS in IBD was assessed in the DSS-induced acute colitis mouse model. Body weight, stool consistency, rectal bleeding, colon length, organ coefficient, cytokine levels in colon tissues, infiltration of immune cells, and colon pathology were evaluated. The anti-inflammatory activity of SMS and related molecular mechanisms were further examined in lipopolysaccharide (LPS)-induced macrophages via assessment of pro-inflammatory cytokine secretion and NF-κB, MAPK, STAT3, and NLRP3 signalling.
UNASSIGNED: SMS significantly ameliorated the severity of disease in acute colitis mice, as evidenced by an improvement in disease activity index, colon morphology, and histological damage. Additionally, SMS reduced pro-inflammatory cytokine production and infiltration of immune cells in colon tissues. Furthermore, in LPS-induced macrophages, we demonstrated that SMS significantly inhibited the production of cytokines and suppressed the activation of multiple pro-inflammatory signalling pathways, including NF-κB, MAPK, and STAT3. SMS also abolished NLRP3 inflammasome activation and inhibited subsequent caspase-1 activation and IL-1β secretion, suggesting a new therapeutic target for the treatment of IBD. These mechanistic findings were also confirmed in in vivo assays.
UNASSIGNED: This study presents the anti-inflammatory activity and detailed molecular mechanism of SMS, in vitro and in vivo. Importantly, we highlight for the first time the potential of SMS as an effective therapeutic agent against IBD.