1.Molecular Biological Mechanism of Damp-Heat Syndrome Based on Intestinal Flora Related Signaling Pathway
Yulong QIE ; Hua JIANG ; Conge TAN ; Xiangdong WANG ; Wenwen XING ; Chen YUAN ; Yujin WANG
World Science and Technology-Modernization of Traditional Chinese Medicine 2023;25(10):3215-3220
Damp-heat syndrome is one of the common syndromes of various clinical diseases.Current studies have shown that intestinal flora is closely related to damp-heat syndrome,but the specific molecular biological mechanism related to intestinal flora and damp-heat syndrome is not yet clear.In this paper,the molecular biological mechanism of damp-heat syndrome is discussed from the perspective of intestinal flora related signaling pathways,so as to provide ideas for the essence of damp-heat syndrome and clinical diagnosis and treatment.
2.Mechanism of Huanglian Wendantang on Damp-heat Type Diabetes Enteropathy Rats Based on TGR5/GLP-1 Signaling Pathway and Intestinal Flora
Yujin WANG ; Yulong QIE ; Hua JIANG ; Chen YUAN ; Xirui DENG ; Xuelian MENG ; Wenli WANG ; Yanjin SU
Chinese Journal of Experimental Traditional Medical Formulae 2025;31(15):10-18
ObjectiveTo explore the mechanism of Huanglian Wendantang on damp-heat type diabetes enteropathy rats based on the G protein coupled bile acid receptor 5/glucagon like peptide-1 (TGR5/GLP-1) signaling pathway and intestinal flora. MethodsA total of 72 male Sprague Dawley (SD) rats were adaptively fed for one week. Twelve SD rats were randomly selected as a blank group and fed with an ordinary diet. The rest of the SD rats were fasted for 12 hours without water. A rat model with damp-heat type diabetes enteropathy was made by left intraperitoneal injection of streptozotocin (55 mg·kg-1) and high sugar and high fat diet (20% sucrose solution + high fat diet) in a humid and hot environment (artificial climate box: temperature 30-34 ℃, relative humidity: 85%-95%). After successful modeling, the rats were randomly divided into a model group, a metformin group (200 mg·kg-1), low-dose, medium-dose, and high-dose Huanglian Wendantang groups (7.10, 14.20, 28.39 g·kg-1), with 12 rats in each group. The normal group and the model group were orally administered with physiological saline once a day for 6 consecutive weeks. During the observation period, the weight and blood glucose levels of rats were measured and recorded weekly. After the administration, fresh feces were collected from rats, and 16S rRNA sequencing technology was used to study the differences and changes in intestinal flora among different groups. The levels of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in the serum of rats were detected by enzyme-linked immunosorbent assay (ELISA), and the pathological morphological changes of colon tissue were examined. The expression of TGR5 and GLP-1 in colon tissue was detected by immunohistochemistry, and the expression of TGR5 and GLP-1 proteins in colon tissue was measured by Western blot. ResultsCompared with the blank group, the model group showed a decrease in body weight, an increase in blood glucose, and significant damp-heat symptoms. The levels of IL-6 and TNF-α in serum were significantly increased (P<0.01). The expression of TGR5 and GLP-1 was decreased (P<0.01), and the pathogenic bacteria were increased. Compared with the model group, the treatment groups exhibited improvements in body weight, blood glucose levels, and damp-heat syndrome in rats. Among them, the high-dose group of Huanglian Wendantang displayed the most significant improvement effect, with significantly reduced inflammation levels (P<0.01) and elevated expression of TGR5 and GLP-1 (P<0.01). Colonic pathological sections showed that Huanglian Wendantang could effectively ameliorate colonic pathological changes. The 16S rRNA sequencing result indicated a significant increase in beneficial bacteria in the treatment groups. ConclusionHuanglian Wendantang can effectively ameliorate the damp-heat symptoms and blood glucose levels in rats with damp-heat type diabetes enteropathy, and it may exert an effect by regulating the TGR5/GLP-1 signaling pathway and intestinal flora disorder.