Folic acid, as a key source of methyl donor in DNA methylation, has been proved to play a beneficial role in inflammation modulation, which is usually impaired in alcoholic liver disease (ALD). However, the role of folic acid in alcoholic liver inflammation and injury remain elusive. In this study, we sought to uncover the potential protective mechanism by which folic acid ameliorates alcoholic liver injury. 100 male C57BL/6J mice were randomly divided into 5 groups: normal saline group, folic acid control group (5 mg per kg BW), ethanol model group (56% v/v, 10 mL per kg BW), folic acid + ethanol group, and 5-Aza + ethanol group (0.1 mL per 20 g BW). Liquor (10 mL per kg BW) was orally administered 1 h after the folic acid treatment for 10 consecutive weeks. The results showed that folic acid-inhibited ethanol-induced serum TG, TC, and LDL elevation attenuated hepatic fat accumulation and maintained ALT at a normal level. 10 weeks of ethanol administration simultaneously upregulated the hepatic proportion of Th17 and Treg cells to different extents and broke the homeostasis of liver immunization. Folic acid limited ethanol-induced inflammatory injury by increasing the frequency of hepatic Treg cells. Importantly, this effect may be caused by decreased DNMT3a, which in turn downregulates the methylated levels of CPG2 and CPG3 in the Foxp3 promoter region, changing the abundance of Foxp3 expression and improving the Th17/Treg imbalance. In summary, our findings demonstrated that folic acid supplementation may relieve ethanol-induced Th17/Treg disbalance through altering Foxp3 promoter methylation patterns, suggesting that folic acid may be a feasible preventive strategy for ALD.

Folic acid intervention changes liver Foxp3 methylation and ameliorates the damage caused by Th17/Treg imbalance after long-term alcohol exposure.

Primary biliary cholangitis (PBC) is an immune-mediated liver disease characterized by cholestasis, biliary injuries, liver fibrosis, and chronic non-suppurative cholangitis. The pathogenesis of PBC is multifactorial and involves immune dysregulation, abnormal bile metabolism, and progressive fibrosis, ultimately leading to cirrhosis and liver failure. Ursodeoxycholic acid (UDCA) and obeticholic acid (OCA) are currently used as first- and second-line treatments, respectively. However, many patients do not respond adequately to UDCA, and the long-term effects of these drugs are limited. Recent research has advanced our understanding the mechanisms of pathogenesis in PBC and greatly facilitated development of novel drugs to target mechanistic checkpoints. Animal studies and clinical trials of pipeline drugs have yielded promising results in slowing disease progression. Targeting immune mediated pathogenesis and anti-inflammatory therapies are focused on the early stage, while anti-cholestatic and anti-fibrotic therapies are emphasized in the late stage of disease, which is characterized by fibrosis and cirrhosis development. Nonetheless, it is worth noting that currently, there exists a dearth of therapeutic options that can effectively impede the progression of the disease to its terminal stages. Hence, there is an urgent need for further research aimed at investigating the underlying pathophysiology mechanisms with potential therapeutic effects. This review highlights our current knowledge of the underlying immunological and cellular mechanisms of pathogenesis in PBC. Further, we also address current mechanism-based target therapies for PBC and potential therapeutic strategies to improve the efficacy of existing treatments.

/pdf/mechanism-based-target-therapy-in-primary-biliary-5gepcrhj.pdf

Mechanism-based target therapy in primary biliary cholangitis: opportunities before liver cirrhosis?

Epigenetics-mediated pathological alternations and their potential in antiphospholipid syndrome diagnosis and therapy.

Primary biliary cholangitis (PBC) is an autoimmune liver disease. The aetiology of PBC remains unclear, and its pathogenesis is complex. Animal models are essential to clarify the pathogenesis of PBC and explore the occurrence of early events.Herein, we review recent research progress in PBC animal models, including genetically modified, chemically inducible, biologically inducible, and protein-immunised models. Although these animal models exhibit several immunological and pathological features of PBC, they all have limitations that constrain further research and weaken their connection with clinical practice.The review will benefit efforts to understand and optimise animal models in order to further clarify PBC pathogenesis and molecular targets for therapeutic interventions. 

Animal models of primary biliary cholangitis: status and challenges

Hypermethylation of the ADIRF promoter regulates its expression level and is involved in NNK-induced malignant transformation of lung bronchial epithelial cells

5-Aza-2-deoxycytidine alleviates the progression of primary biliary cholangitis by suppressing the FoxP3 methylation and promoting the Treg/Th17 balance.

Prophylactic transcatheter angiographic embolization reduces Forrest IIa ulcer rebleeding: A retrospective study.

The utility model discloses a filtering device for extracting plasmids. the device comprises a filter column, a filter element, an upper plate, a lower plate, a left plate, a right plate, a rear plate, a waste filter device, a first support plate, a test tube plate, a splash-proof device, a second support plate, a test tube, a spring, an ultraviolet lamp and a switch, wherein the filter column isinserted into the upper plate, the filter element is arranged below the filter column, the left side of the rear plate is fixedly connected with the right plate, the right plate is fixedly connected with the left plate, the upper surface of the rear plate is fixedly connected with the upper plate, and the lower surface is fixedly connected with the lower plate to form a box body. According to thefiltering device for plasmid extraction, the waste liquid device is additionally arranged and used for treating messy waste liquid, and the splash-proof device is arranged below the filtering pipe andcan prevent liquid from splashing. The waste liquid devices are placed on the supporting plates which are evenly arranged on the inner sides of the left plate and the right plate, and the waste liquid devices with different depths can be placed. Springs are arranged on the left sides of the inserting holes of the test tube plate and can contain test tubes of different sizes. Ultraviolet lamps arearranged at the upper ends of the inner sides of the left plate and the right plate and can sterilize filtrate.

Filtering device for extracting plasmids

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5-Aza-2-deoxycytidine alleviates the progression of primary biliary cholangitis by suppressing the FoxP3 methylation and promoting the Treg/Th17 balance.

Prophylactic transcatheter angiographic embolization reduces Forrest IIa ulcer rebleeding: A retrospective study.

Filtering device for extracting plasmids