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Fatty liver disease is a disease manifested with excessive alcohol intake and obese. Importantly, hydrogen sulfide (H2S) has been revealed to participate in the progression of fatty liver; however, the underlying mechanism has not been clearly elucidated yet. In this study, we aimed to investigate the effects of exogenous H2S on fatty liver ischemia–reperfusion injury (IRI) through mediating class A scavenger receptor (SRA) pathway in rats. By determining endoplasmic reticulum stress (ERS)‐related factors, autophagy markers and apoptosis‐related factors in liver tissue and liver function, levels of oxidative stress, inflammatory factors, and hepatocyte apoptosis, the effects of H2S on IRI‐induced autophagy, oxidative stress, and inflammation were all examined in rat model of fatty liver IRI. Results from obtained data showed that H2S decreased the expression of SRA, Grp78, PERK, CHOP, and Caspase‐3, and increased that of LC3‐II/LC3‐I, in addition to alleviating the pathological changes of liver and reducing the levels of ALT, AST, LDH TBARS, and MDA. Moreover, H2S decreased the levels of oxidative stress, the expression of pro‐inflammatory factors including tumor necrosis factor α, interleukin 1, and interleukin 6, and the apoptosis of hepatocytes. Our findings suggested exogenous H2S could reduce ERS by mediating the SRA pathway and protect liver function by inducing autophagy, and protect against IRI by reducing oxidative stress and inflammation. [ABSTRACT FROM AUTHOR]

Objectives: To investigate the role of Morinda officinalis polysaccharide (MOP) in the protein expression of the Wnt/β-catenin signaling cascade during the osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs), and to elucidate the mechanisms by which MOP enhances osteogenic differentiation at the cellular level., Methods: BMSCs were isolated and cultured using the whole bone marrow adherence method, followed by flow cytometry for the detection of BMSC marker antigens. Two groups were prepared: a low-dose MOP (L-MOP, 10 µg/mL) group and a high-dose MOP (H-MOP, 40 µg/mL) group. MTT assays and cell clone formation assays were performed to evaluate the effects of different MOP doses on BMSC proliferation. Alizarin red staining (ARS) and alkaline phosphatase (ALP) staining were conducted to assess the impact of varying MOP doses on nodule calcification and ALP activity in BMSCs. Additionally, western blot assays were carried out to determine the effects of different MOP concentrations on the expression levels of osteogenesis-related factors and Wnt/β-catenin pathway proteins in BMSCs., Results: Highly purified BMSCs were successfully extracted. Subsequent assays demonstrated that BMSCs exhibited enhanced proliferation at all MOP doses, particularly at the H-MOP dose, compared to the control group. Both L-MOP and H-MOP increased calcium content and ALP activity in BMSCs, as well as elevated the expression of osteogenic factors and Wnt/β-catenin pathway proteins compared to the blank control group. However, the addition of Dickkopf-1 (DKK1) significantly reduced BMSC proliferation and osteogenic differentiation compared to the H-MOP group., Conclusions: MOP can enhance BMSC proliferation and osteogenic differentiation by activating the Wnt/β-catenin signaling pathway., Competing Interests: None., (AJTR Copyright © 2024.)