The American journal of Chinese medicine
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Ulcerative colitis (UC), one among other refractory diseases worldwide, has shown an increasing trend of progression to colorectal cancer in recent years. In the treatment of UC, traditional Chinese medicine has demonstrated good efficacy, with a high cure rate, fewer adverse effects, great improvement in the quality of patient survival, and reduction in the tendency of cancerous transformation. ⋯ We also summarized the mechanisms of action of various Chinese medicines (active ingredients or extracts) and herbal formulas, through signaling pathways and gut microbiota, with the expectation that they can provide references and evidence for treating UC and preventing inflammation-associated colorectal cancer by traditional Chinese medicine. We illustrate that multiple signaling pathways, such as TLR4, STAT3, PI3K/Akt, NF-[Formula: see text]B, and Keap1/Nrf2, can be inhibited by Chinese herbal treatments through the combined regulation of signaling pathways and gut microbiota, which can act individually or synergistically to inhibit intestinal inflammatory cell infiltration, attenuate gut oxidative responses, and repair the intestinal barrier.
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Irritable bowel syndrome (IBS) is the functional gastrointestinal disorder, characterized by abdominal pain and altered bowel habits. The interest in intestinal immune activation as a potential disease mechanism for IBS has increased exponentially in recent years. This study was designed to summarize the Chinese herbal medicine (CHM) that potentially exert protective effects against IBS through inhibition of intestinal immune activation. ⋯ The mechanisms mainly focused on the gut microbiota disorder induced alteration of the PGE2/COX2/SERT/5-HT, TLR4/MyD88/NF-κB, and BDNF/TrkB pathways. Most of the CHM alleviated IBS through interventions of intestinal immune activation via gut microbiota related to the TLR4/MyD88/NF-κB and SCF/c-kit pathways. We hope this review will provide some clues for the further development of novel candidate agents for IBS and other intestinal immune disorders.
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Cellular senescence is an adverse factor in the development of pulmonary fibrosis (PF). Ginsenoside Rb1 has been found to inhibit both cellular senescence and PF. This study aimed to elucidate the molecular mechanisms by which ginsenoside Rb1 regulates cellular senescence and PF. ⋯ As expected, ginsenoside Rb1 alleviated ARD-induced senescence and fibrosis in MRC-5 cells by activating the NRF2/QKI/SMAD7 axis. Therefore, it was found that ginsenoside Rb1 mitigates cellular senescence and fibrosis during PF progression by activating the NRF2/QKI/SMAD7 axis. This study provides a potential therapeutic strategy for the treatment of PF and elucidates its mechanism of action.