Effect of huankuile on colon injury in rats with ulcerative colitis by reducing TNF-α and MMP9.

OBJECTIVE: To explore the mechanism of huankuile (HKL) in colon injury repair in rats with ulcerative colitis (UC). METHODS: Fifty SPF Wistar male rats were divided randomly into a normal group, a negative control group, an HKL intervention group ('HKL group') and a 5-aminosalicylic acid intervention group ('5-ASA group'). After 14 days of intervention with corresponding drugs, pathological scores were obtained using the results of immunohistochemical staining; morphological changes were observed by hematoxylin-eosin staining, and the mRNA expression levels of tumour necrosis factor-α (TNF-α), matrix metalloproteinase 9 (MMP9) and interleukin-13 (IL-13) were detected by real-time quantitative PCR. RESULTS: After the successful construction of the rat model, it was compared with the rats in the normal group. In the negative group, it was found that the expression of TNF-α and MMP9 was significantly increased in the colonic mucosal epithelia of the rats, the pathological score was significantly increased (P < 0.05), and the mRNA expression levels of TNF-α, MMP9 and IL-13 were increased (P < 0.05). After treatment with HKL, the colonic morphology of the rats returned to normal, the expression of TNF-α and MMP9 in the colonic mucosal epithelium of the rats returned to normal, the pathological score grade was significantly reduced (P < 0.05), and the mRNA expression levels of TNF-α, MMP9 and IL-13 were reduced; these results were largely consistent with those of the normal group, with no statistically significant difference. CONCLUSION: HKL effectively improved the general symptoms and tissue injury in UC rats, and the therapeutic effect was better than that of 5-ASA group. Ulcerative colitis in rats increased the expression of TNF-α, MMP9 and IL-13. HKL repaired UC-induced colonic injury in rats by decreasing the expression of TNF-α, MMP9 and IL-13.

Lactobacillus acidophilus and HKL Suspension Alleviates Ulcerative Colitis in Rats by Regulating Gut Microbiota, Suppressing TLR9, and Promoting Metabolism.

Ulcerative colitis (UC) is a chronic non-specific inflammatory bowel disease with complex pathogenesis. The intestinal flora disturbance affects the homeostasis of the intestinal environment, leading to metabolic imbalance and immune abnormalities of the host, contributing to the perpetuation of intestinal inflammation. We suggest that the combination of anti-inflammatory therapy and the regulation of intestinal flora balance may help in the treatment process. Previously, we used a combination treatment consisting of Lactobacillus acidophilus (Lac) and Chinese medicine Huan Kui Le (HKL) suspension in a UC rat model, where the combined intervention was more effective than either treatment alone. Herein, the mechanism of action of this combined treatment has been investigated using 16S rRNA sequencing, immunohistochemistry, and ELISA methods in the colon, and untargeted metabolomics profiling in serum. Colon protein expression levels of IL-13 and TGF-ß were upregulated, whereas those of TLR9 and TLR4 were downregulated, consistent with an anti-inflammatory effect. In addition, gut microbiota structure changed, shown by a decrease in opportunistic pathogens correlated with intestinal inflammation, such as Klebsiella and Escherichia-Shigella, and an increase in beneficial bacteria such as Bifidobacterium. The latter correlated positively with IL-13 and TGF-ß and negatively with IFN-γ. Finally, this treatment alleviated the disruption of the metabolic profile observed in UC rats by increasing short-chain fatty acid (SCFA)-producing bacteria in the colonic epithelium. This combination treatment also affected the metabolism of lactic acid, creatine, and glycine and inhibited the growth of Klebsiella. Overall, we suggest that treatment combining probiotics and traditional Chinese medicine is a novel strategy beneficial in UC that acts by modulating gut microbiota and its metabolites, TLR9, and cytokines in different pathways.

Research on Establishment of Abnormal Phlegmatic Syndrome with Premature Ovarian Failure Rat Model and Effects of Balgham Munziq Treatment.

This study aimed to establish and explore the biological basis of abnormal phlegmatic syndrome with premature ovarian failure (POF) model in rats based on the Uighur medicine (UM) in the first place and investigate the effects of unique herbal medicine, Balgham Munziq (BMq). Mature female Wistar rats were fed with spinach and coriander in cold and humid condition for approximately 20 weeks until abnormal phlegmatic syndrome (APS) model was established. When APS model was confirmed by Uighur medical experts, APS with POF disease rats were subdivided into APS with POF disease model group and APS with POF disease treated with BMq group; the rest of them were subdivided into APS model group and APS treated with BMq group. The results show that biological characteristics of animals in the course of modeling period were in accordance with clinical features of abnormal phlegmatic syndrome (APS) in Uighur medicine. Herbal medicine BMq not only reverted reproductive hormone levels disorders but also improved the function of hypothalamic-pituitary-ovarian axis and regulated secretion of monoamine neurotransmitters. APS is most likely to cause pathological changes of hypothalamic-pituitary-ovarian axis and lead to the occurrence of POF and BMq is effective in the treatment of APS with POF disease.