Colorectal cancer (CRC) is a substantial global health challenge, with current treatments often leading to relapse and metastasis. Curcumin, a natural compound derived from turmeric, has shown promise in cancer therapy; however, its mechanisms in CRC are not fully understood. The present study aimed to investigate the role of curcumin in inducing pyroptosis, a form of inflammatory cell death, through caspase‑1 activation in CRC cells. Human CRC cell lines (HCT‑116 and SW480) and normal colon epithelial cells (FHC) were treated with curcumin at varying concentrations. Cell viability, migration and invasion were assessed using Cell Counting Kit‑8, wound healing and Transwell assays, respectively. Pyroptosis was evaluated through lactate dehydrogenase (LDH) release, TUNEL staining and western blot analysis of pyroptosis‑related proteins (caspase‑1, gasdermin D, nucleotide‑binding oligomerization domain‑like receptor protein 3, IL‑1β and IL‑18). The role of caspase‑1 was further examined using the inhibitor VX‑765. Curcumin significantly reduced CRC cell viability, migration and invasion in a dose‑dependent manner. In addition, it induced pyroptosis, as evidenced by cell membrane swelling, increased LDH release and upregulation of pyroptosis‑related proteins. Inhibition of caspase‑1 with VX‑765 attenuated these effects, confirming the role of caspase‑1 in curcumin‑induced pyroptosis. In conclusion, curcumin may exert anti‑CRC effects by inducing caspase‑1‑mediated pyroptosis, highlighting its potential as a therapeutic agent. These findings suggest that curcumin could be integrated into current CRC treatment strategies, particularly in targeting pyroptosis to enhance tumor suppression.

This study explores American patients’ understanding of traditional Chinese medicine (TCM) in the late 19^th century by referring to letters from American patients recorded in The Science of Oriental Medicine, written by Tan Fuyuan (谭富园), a Chinese medicine doctor working in the United States in the late Qing dynasty. Identifying a focus on significant effects, pulse diagnosis, herbal teas, dietary control, and long-term treatment, the results also discussed the differences between TCM and Western medicine in simple terms to show that the “ideological” spread of TCM was based on its curative effect. However, the “theoretical” spread of TCM requires more of intercultural exchanges.

Xin-Jia-Tong-Xie-Yao-Fang (XJTXYF) is a proven prescription for managing diarrhea-predominant irritable bowel syndrome (IBS-D), which is a prevalent functional gastrointestinal disorder. However, the underlying mechanism of XJTXYF remains unclear. This study aims to explore the material basis and potential mechanisms of XJTXYF against IBS-D. The constituents of XJTXYF were identified by UPLC-Q-TOF-MS/MS, and potential targets and pathways were screened by network pharmacology. Changes in the intestinal microbiome and fecal butyric acid levels after XJTXYF administration were analyzed through 16S rRNA sequencing and HPLC respectively. The abdominal withdrawal reflex score, serum levels of FITC-D and the expression of intestinal epithelial tight junction proteins, as well as the activity of the PI3K/Akt pathway were assessed. In-vitro experiments involved silencing GPR109A using small interfering RNA and inducing barrier damage with LPS pre-treatment in the Caco-2 cell line. Barrier function was evaluated by FITC-D permeability and tight junction protein expressions. The activity of the PI3K/Akt pathway was determined through Western blotting analysis. The major active compounds of XJTXYF identified by UPLC-Q-TOF-MS/MS include Saikosaponin C, Hesperetin, Neohesperidin, Albiflorin, Quercetin and so on. The PI3K/Akt signaling pathway was predicted by network pharmacology as a potential target of XJTXYF in treating IBS-D. Animal experiments demonstrated that XJTXYF could increase body weight, improve visceral hypersensitivity, rebalance gut flora dysbiosis and upregulate fecal butyric acid content in IBS mice. The XJTXYF also showed the abilities of intestinal barrier repairment and PI3K/Akt pathway suppression. Fecal microbiota transplantation and the positive controls (NaB and Clostridium Butyricum) verified that a causal relationship existed between gut microbiome changes and IBS-D improvement after XJTXYF treatment. In-vitro experiments revealed the role of butyrate in barrier protection via PI3K/Akt inhibition. Overall, in this study, we revealed that XJTXYF could restore intestinal barrier function through microbial butyrate mediated PI3K/Akt inhibition and improve IBS-D symptoms.