Ulcerative colitis (UC) is an inflammatory disease of the intestinal mucosa, and its incidence is steadily increasing worldwide. As a traditional Chinese medicinal insect, Periplaneta americana has been broadly utilized in clinical practice to treat wound healing. The tryptophan (Trp), tryptamine (Try), and 1,2,3,4-tetrahydrogen-β-carboline-3-carboxylic acid (Thcc) identified from P. americana concentrated ethanol-extract liquid (PACEL) exhibit significant cell proliferation-promoting and anti-inflammatory effects in the treatment of UC, but the mechanism involved remains obscure. Here, a dextran sulfate sodium (DSS)-induced UC mouse model was used to investigate the efficacy of high/low doses of PACEL, Trp, Try, and Thcc. Transcriptome sequencing was employed to detect the gene expression in the mouse intestine. The results showed that high doses of PACEL, Trp, Try, and Thcc could significantly improve weight loss and diarrhea, notably in the PACEL and Trp groups. Transcriptome analysis indicated that statistically changed genes in four treatment groups were specifically enriched in the immune system. Of these, the integrated analysis identified six hub genes (IL1β, CCL4, CXCL5, CXCR2, LCN2, and MMP9) regulated by NF-κB, which were significantly downregulated. This study investigates the molecular mechanisms underlying the UC treatment properties of indole analogues from PACEL, potentially through the inhibition of the NF-κB signaling pathway.

The pathological assessment of diabetes mellitus (DM) in humans is frequently confounded by glucose-lowering therapies. Untreated spontaneously diabetic rhesus macaques (Macaca mulatta) provide a valuable model for elucidating the authentic pathology of the disease. In this study, we performed histopathological, immunohistochemical, and transcriptomic analyses on the pancreas, liver, and skeletal muscle of a spontaneous diabetic macaque alongside healthy controls. The results demonstrate that the pancreas exhibited the most severe histopathological damage, with extensive acinar destruction, apoptosis, and prominent IL-17-mediated inflammation, underpinned by activation of the p53 signaling pathway and suppression of exocrine secretion genes. In the liver, damage is driven primarily by innate immune activation and metabolic inflammation, manifesting as metabolic dysfunction-associated steatotic liver disease (MASLD)-like steatotic lesions and insulin resistance-related cytokine expression. In skeletal muscle, endoplasmic reticulum stress emerges as a key molecular event linked to muscle fiber atrophy. Cross-species comparison with human T2DM pancreatic data further identified 20 conserved differentially expressed genes (DEGs) involved in insulin/IGF signaling and chronic inflammation. Collectively, these findings provide a multi-organ perspective on diabetes-induced pathological and transcriptional alterations and underscore the translational relevance of the macaque model for human diabetes research.