Treatment of gastric ulcer, traditional Chinese medicine may be a better choice.

ETHNOPHARMACOLOGICAL RELEVANCE: Gastric ulcer (GU) is the injury of the gastric mucosa caused by the stimulation of various pathogenic factors penetrating the deep mucosal muscle layer. An increasing number of studies have shown that traditional Chinese medicine (TCM) is highly effective in treating GU due to its multitarget, multilevel, and multi-pathway effects. AIM OF THE STUDY: To review the latest research progress in the treatment of GU by TCM, including clinical and experimental studies, focusing on the target and mechanism of action of drugs and providing a theoretical basis for the treatment of GU by natural herbs. MATERIALS AND METHODS: Electronic databases (PubMed, Elsevier, Springer, Web of Science, and CNKI) were searched using the keywords "gastric ulcer", "gastric mucosal lesion", "TCM" and or paired with "peptic ulcer" and "natural drugs" for studies published in the last fifteen years until 2023. RESULTS: TCM, including single components of natural products, Chinese patent medicines (CPM), and TCM decoction, is expected to treat GU by regulating various mechanisms, such as redox balance, inflammatory factors, angiogenesis, gastric mucosal protective factors, intestinal flora, apoptosis, and autophagy. CONCLUSIONS: We discussed and summarized the mechanism of TCM in the treatment of GU, which provided a sufficient basis for TCM treatment of GU.

Xiangshao Decoction alleviates gastric mucosal injury through NRF2 signaling pathway and reduces neuroinflammation in gastric ulcer rats.

BACKGROUND: A type of gastric mucosal injury disease known as gastric ulcer (GU) is clearly connected to the aberrant release of gastric acid. Traditional botanicals have the potential for anti-inflammation, anti-oxidation, and other multitarget therapies, as well as being safe. PURPOSE: The purpose of this study was to investigate the potential effects of Xiangshao Decoction (XST) on gastric mucosal injury in GU rats and to explore the possible molecular mechanisms. METHODS: After identifying XST and its components, we established GU rats and cell models by acetic acid and H2O2 induction, respectively. SOD and MDA indexes in gastric tissues and GES-1 cells, and the serum levels of BDNF, ALT, and AST were detected with relevant kits, changes of the gastric mucosa were observed and recorded, and gastric tissue pathology was observed by H&E staining. The production of ROS in GES-1 cells was detected by fluorescent probes. Cell transfection techniques were used to silence or overexpress NRF2. The mRNA or protein expressions of NRF2, KEAP1, NQO1, HO-1, SOD2, IL-1ß, IL-6, TNF-α, IBA1, GFAP, or γ-H2AX in the gastric tissue, hippocampus, or GES-1 cells were measured via qPCR, Western blot, immunofluorescence staining, or immunohistochemical staining. RESULTS: The pH of gastric acid, ulcer score, and pathological damage score in GU rats could be reversed by XST administration. Expressions of IL-1ß, IL-6, and TNF-α in the gastric mucosal tissues and the hippocampus of GU rats after administration of XST were down. Expressions of NRF2, NQO1, HO-1, SOD2, etc. in the gastric mucosal tissues and BDNF in the hippocampus were up-regulated. The production of ROS and MDA and the expressions of IL-1ß, IL-6, TNF-α, and KEAP1 in H2O2-induced GES-1 cells were significantly reduced after XST intervention, while the activities of SOD and the expression of NRF2, NQO1, HO-1, and SOD2 were significantly increased, and these could be blocked by silencing NRF2 expression. CONCLUSIONS: XST can improve oxidative stress injury and inflammatory response in GU rats and cell models, and its mechanism is mediated by the NRF2 signaling pathway.

Hesperidin inhibits lung fibroblast senescence via IL-6/STAT3 signaling pathway to suppress pulmonary fibrosis.

BACKGROUND: Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive, and fatal lung disease with obscure pathogenesis. Increasing evidence suggests that cellular senescence is an important mechanism underlying in IPF. Clinical treatment with drugs, such as pirfenidone and nintedanib, reduces the risk of acute exacerbation and delays the decline of pulmonary function in patients with mild to moderate pulmonary fibrosis, and with adverse reactions. Hesperidin was previously shown to alleviate pulmonary fibrosis in rats by attenuating the inflammation response. Our previous research indicated that the Citrus alkaline extracts, hesperidin as the main active ingredient, could exert anti-pulmonary fibrosis effects by inhibiting the senescence of lung fibroblasts. However, whether hesperidin could ameliorate pulmonary fibrosis by inhibiting fibroblast senescence needed further study. PURPOSE: This work aimed to investigate whether and how hesperidin can inhibit lung fibroblast senescence and thereby alleviate pulmonary fibrosis METHODS: Bleomycin was used to establish a mouse model of pulmonary fibrosis and doxorubicin was used to establish a model of cellular senescence in MRC-5 cells in vitro. The therapeutic effects of hesperidin on pulmonary fibrosis using haematoxylin-eosin staining, Masson staining, enzyme-linked immunosorbent assay, immunohistochemistry, western blotting and quantitative Real-Time PCR. The anti-senescent effect of hesperidin in vivo and in vitro was assessed by western blotting, quantitative Real-Time PCR and senescence-associated ß-galactosidase RESULTS: We demonstrated that hesperidin could alleviate bleomycin-induced pulmonary fibrosis in mice. The expression level of senescence marker proteins p53, p21, and p16 was were downregulated, along with the myofibroblast marker α-SMA. The number of senescence-associated ß-galactosidase-positive cells was significantly reduced by hesperidin intervention in vivo and in vitro. In addition, hesperidin could inhibit the IL6/STAT3 signaling pathway. Furthermore, suppression of the IL-6/STAT3 signaling pathway by pretreatment with the IL-6 inhibitor LMT-28 attenuating effect of hesperidin on fibroblast senescence in vitro. CONCLUSIONS: These data illustrated that hesperidin may be potentially used in the treatment of IPF based on its ability to inhibit lung fibroblast senescence.

[Protective effects of n-butanol extract of Potentilla anserina on acute myocardial ischemic injury in mice].

OBJECTIVE: To investigate the protective effects of the n-butanol extract of Potentilla anserina L. (NP) on pituitrin-induced acute myocardial ischemic injury in mice. METHODS: Ninety healthy female mice were randomly divided into normal control group, untreated group, Salvia miltiorrhiza group and low-, medium- and high-dose NP groups. Except for the normal control group, the mice were intraperitoneally injected with pituitrin (20 U/kg) to induce acute myocardial ischemic injury. Thirty minutes after induction, electrocardiogram was monitored, and height of the J spot was measured also. Activities of lactate dehydrogenase (LDH), creatine kinase (CK) and superoxide dismutase (SOD) and content of malondialdehyde (MDA) in serum of the mice were detected. The degree of myocardial ischemic injury in mice was observed by Nagar-Olsen staining. RESULTS: The moving up of J spots in the treated groups was significantly inhibited when comparing with the untreated group (P<0.01). Compared with untreated group, high- and medium-dose NP and Salvia miltiorrhiza could significantly decrease the activities of LDH, CK (P<0.01, P<0.05), increase the SOD activity (P<0.01) and decrease the content of MDA (P<0.05). However, no significant difference was observed between low-dose NP group and untreated group (P>0.05). Nagar-Olsen staining showed that high- and medium-dose NP and Salvia miltiorrhiza could significantly diminish the areas of cardiac muscles injured by ischemia, but low-dose NP had no effect on that. CONCLUSION: NP has a remarkable protective effect on acute myocardial ischemic injury in mice.