Background:Autoimmune gastritis(AIG)is a CD4+T cell-mediated immune disease.In recent years,with increased awareness and understanding of the condition,reports of AIG cases in China have been gradually increasing.Aims:To analyze and summarize the clinical characteristics of AIG for better disease recognition and diagnosis.Methods:Data on AIG patients diagnosed at the First Affiliated Hospital of Zhejiang Chinese Medical University from August 2018 to December 2023 were collected and analyzed for their clinical,laboratory,endoscopic,and pathological features.Results:A total of 161 AIG patients were included,with the mean age of 56.81 years old,63 were males and 98 females.Most of the patients exhibited no characteristic clinical symptoms.The laboratory measurements were as follows:gastrin-17,44.68 pmol/L;pepsinogen(PG)Ⅰ,38.61 μg/L;PG Ⅱ,10.41 μg/L;PGⅠ/Ⅱ ratio,32.1;vitamin B12,344.45 pmol/L;and hemoglobin,125.15 g/L.The positivity rates of thyroglobulin antibody and thyroid peroxidase antibody were 46.0%and 30.0%,respectively.The main comorbid autoimmune diseases were Hashimoto's thyroiditis(8.1%)and rheumatoid arthritis(5.0%).One hundred and seven cases exhibited the"reverse atrophy"phenomenon,while 54 cases showed pan-gastric atrophy,predominantly in the fundus and body.Fifteen cases were diagnosed as gastric neuroendocrine tumors(NET)or gastric carcinoma.Pathological analysis of 90 gastric mucosal specimens showed 24 cases of lymphocyte and plasma cell infiltration without significant atrophy,42 cases of glandular atrophy and lymphocyte infiltration,and 24 cases of enterochromaffin cell hyperplasia and the formation of endocrine micro-nests.Conclusions:AIG is more common in middle-aged and elderly individuals,with a slightly higher prevalence in females and a frequent association with anemia.It should be suspected in patients with low PGⅠ level and hypergastrinemia.Due to the increased risk of gastric adenocarcinoma and NETs,regular endoscopic monitoring is recommended.

Background:Autoimmune gastritis(AIG)is a CD4+T cell-mediated immune disease.In recent years,with increased awareness and understanding of the condition,reports of AIG cases in China have been gradually increasing.Aims:To analyze and summarize the clinical characteristics of AIG for better disease recognition and diagnosis.Methods:Data on AIG patients diagnosed at the First Affiliated Hospital of Zhejiang Chinese Medical University from August 2018 to December 2023 were collected and analyzed for their clinical,laboratory,endoscopic,and pathological features.Results:A total of 161 AIG patients were included,with the mean age of 56.81 years old,63 were males and 98 females.Most of the patients exhibited no characteristic clinical symptoms.The laboratory measurements were as follows:gastrin-17,44.68 pmol/L;pepsinogen(PG)Ⅰ,38.61 μg/L;PG Ⅱ,10.41 μg/L;PGⅠ/Ⅱ ratio,32.1;vitamin B12,344.45 pmol/L;and hemoglobin,125.15 g/L.The positivity rates of thyroglobulin antibody and thyroid peroxidase antibody were 46.0%and 30.0%,respectively.The main comorbid autoimmune diseases were Hashimoto's thyroiditis(8.1%)and rheumatoid arthritis(5.0%).One hundred and seven cases exhibited the"reverse atrophy"phenomenon,while 54 cases showed pan-gastric atrophy,predominantly in the fundus and body.Fifteen cases were diagnosed as gastric neuroendocrine tumors(NET)or gastric carcinoma.Pathological analysis of 90 gastric mucosal specimens showed 24 cases of lymphocyte and plasma cell infiltration without significant atrophy,42 cases of glandular atrophy and lymphocyte infiltration,and 24 cases of enterochromaffin cell hyperplasia and the formation of endocrine micro-nests.Conclusions:AIG is more common in middle-aged and elderly individuals,with a slightly higher prevalence in females and a frequent association with anemia.It should be suspected in patients with low PGⅠ level and hypergastrinemia.Due to the increased risk of gastric adenocarcinoma and NETs,regular endoscopic monitoring is recommended.

AIM: To investigate the protective affect of salvianolic acid A on palmitic acid-induced lipotoxicity in hepatocyte and its potential molecular mechanism. METHODS: The lipotoxicity model of AML12 hepatocytes induced by PA was established. Different concentrations of Sal A (20, 40, 80, 120 μmol/L) were intervened. The hepatocyte injury was detected by the Lactate dehydrogenase (LDH) method, the intracellular triglyceride (TG) content was detected by enzyme assay and the lipid droplets were observed by Bodipy staining, cell viability was detected by MTT, Intracellular reactive oxygen species (ROS) were detected by 2'eci'- dichlorofluorescein diacetate (DCFH-DA) and fluorescence microscope. Mitochondrial membrane potential was detected by rhodamine 123 and fluorescence microscope. The expression of phosphorylation of AMP-activated protein kinase (AMPK) protein and silent information regulator 1 (SIRT1) protein were observed by Western blot. RESULTS: Model of hepatocyte lipotoxicity was established after intervented for 12 h in vitro with PA (0.5 mmol/L). Different concentrations of Sal A could significantly reduce the lipid deposition and hepatocytes injury induced by PA (P<0.05), and the protective effect was dose-dependent. Secondly, Sal A could significantly improve cell mitochondrial membrane potential (P<0.01) and abate the ROS level of hepatocytes induced by PA (P<0.01). In addition, PA could significantly inhibit AMPK and SIRT1 protein expression (P<0.05). Salvianolic acid A can significantly up-regulate SIRT1 and AMPK protein expression (P<0.05). CONCLUSION: Sal A improves PA induced lipotoxicity in hepatocyte, AMPK and SIRT1 may be a potential molecular target.

AIM: To reveal the ameliorative effect of salvianolic acid A on palmitie acid-induced lipotoxicity in H9C2 cells and to explore its potential molecular mechanisms preliminarily. METHODS: H9C2 cell were induced by palmitie acid to establish a lipotoxicity model, while salvianolic acid A was added prior to palmitie acid treatment. Lactate dehydrogenase (LDH) was employed to detect cell damage. Cell counting Kit-8 was used to detect cell viability. The changes of mitochondrial membrane potential in cardiomyocyte were observed by rhodamine 123 staining. The molecular mechanisms of the ameliorative effect of salvianolic acid A was analyzed by Western Blotting. RESULTS: Palmitie acid at a concentration of 400 μmol/L significantly caused lipotoxicity damage to H9C2 cells (P<0.05). There was no cytotoxic effect of different concentrations of salvianolic acid A (10, 20, 40, 80 μmol/L) treatment on H9C2 cells (P>0.05). Salvianolic acid A intervention significantly improved lipotoxicity-induced cell death and reduction of cell mitochondrial membrane potential (P<0.05). The activation of toll-like receptor 4 (TLR4) significantly enhanced lipotoxicity-induced cell damage (P<0.05), while inhibition of TLR4 significantly reduced palmitie acid-induced lipotoxicity (P<0.05). In addition, salvianolic acid A effectively inhibited the upregulation of TLR4 and the downstream c-Jun N-terminal kinase (JNK MAPK) of TLR4 by palmitie acid treatment (P<0.05). CONCLUSION: Salvianolic acid A effectively improves lipotoxicity-induced cardiomyocyte damage. The inhibition of p38 signaling pathway is potentially involved in its protective effect. The protective effect may be related to the inhibition of TLR4/JNK MAPK signaling pathway, providing a potential molecular target for the prevention and treatment of lipotoxic cardiomyopathy.