👤 Peng Xue Biao

Lipid metabolism may be linked to chronic gastritis, but its causal role remains unclear. While current research emphasizes inflammation, mucosal changes, immune regulation, genetics, and the gut microbiota, the contribution of lipid metabolism is understudied. This study aims to evaluate the impact of serum lipids and the mechanistic roles of lipid-lowering drug targets in chronic gastritis. We conducted a cross-sectional study using data from real world. Multivariable logistic regression was performed to assess the association between serum lipid profiles and gastritis. Mendelian randomization (MR) analyses based on genome-wide association study (GWAS) datasets were performed to detect the causal relationship of serum lipids, plasma lipid species, and lipid-lowering drug targets. Experimental validation was conducted using high-fat diet (HFD)-fed mice and chemically induced CAG rat models. Four thousand sixty one person, including 1,023 patients with chronic atrophic gastritis (CAG), 1,742 with non-atrophic gastritis (NAG), and 1,296 as healthy population were included in the analysis. Through covariates adjustment, TC, ApoA1, and HDL-C showed to be associated with an increased risk of chronic gastritis, whereas TG exhibited a protective effect. MR analysis confirmed a significant inverse causal relationship between TG and gastritis (OR = 0.889, 95% CI: 0.825-0.958). Ten plasma lipid species and lipid-lowering gene targets, including LPL and APOC3, were identified as causally associated with disease risk. Mediation analysis revealed six plasma lipid species as potential intermediaries linking genetic variation to gastritis. In vivo experiments demonstrated progressive hepatic steatosis and mild gastric mucosal changes in HFD-fed mice. Immunohistochemical analysis further revealed a significant reduction in LPL and APOC3 expression in gastric tissue (P < 0.05). In the CAG rat model, histological analysis revealed hepatocyte disarray, edema, and gastric mucosal atrophy. Elevated levels of TNF-α, IL-6, IL-1β and decreased levels of GAS-17 and PG I/II were also observed (P < 0.05). Western blot analyses further confirmed the downregulation of LPL and APOC3 expression in gastric tissue (P < 0.05). This study provides genetic and experimental evidence, supporting a causal role of lipid metabolism in chronic gastritis. LPL and APOC3 are implicated in its pathogenesis, highlighting potential lipid-targeted strategies for prevention and treatment. Show less

Psoriasis is a common chronic immune-mediated inflammatory skin disorder characterized by erythematous silvery scaling of the skin and associated severe itching. Reports indicate that psoriasis is affecting about 2% of the world population and life quality in a way that limits the patient activity and thereby productivity in a community. Therefore, determining appropriate therapeutics for psoriasis would make a difference in the lives of the patients and their communities. To address this, scientists have been working on different biological agents, such as interleukins and their antagonists, to regulate the common inflammatory process in psoriasis. For the current research project, serum was collected from 26 psoriatic patients and another 26 health controls, and the serums were examined for the level of IL-30 to determine differences among the tested groups and to investigate a possible correlation between IL-30 and psoriasis area severity index (PASI). The study delineated differences of the IL-30 among the groups and a positive correlation between IL-30 and PASI among the psoriatic cases, which insights a need for further studies that include a large scale of participants to fully elucidate the involvement of IL-30 in psoriasis. Show less