Psychosocial-Stress, Liver Regeneration and Weight Gain: a Conspicuous Pathophysiological Triad

Background Long working hours causes several health risks, but little is known about its effects on the liver. This study aimed to examine the correlation between working hours and abnormal liver enzyme levels. Methods We used data from the Korea National Health and Nutrition Examination Survey IV–VII. For the final 15,316 study participant, the information on working hours was obtained through questionnaires, and liver enzyme levels, consisting of serum levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT), through blood tests. The relationship between weekly working hours and abnormal levels of liver enzymes was analyzed using multiple logistic regression, and a trend test was also conducted. Results In male, working ≥ 61 hours per week was significantly associated with elevated AST and ALT levels compared with working 35–52 hours per week. Even after adjusting for covariates, the odds ratios (ORs) of abnormal AST and ALT increased by 1.51 (95% confidence interval: 1.20–2.05) and 1.25 (1.03–1.52), respectively, and a dose-response relationship was observed. This association was more prominent among the high-risk group, such as those aged > 40 years, obese individuals, worker on non-standard work schedule, pink-collar workers, or temporary worker. No correlation was observed in female. Conclusions Long working hours are associated with abnormal liver function test results in male. Strict adherence to statutory working hours is necessary to protect workers’ liver health.

Despite the progress that has occurred in recent years in the development of therapies to treat painful and inflammatory diseases, there is still a need for effective and potent analgesics and anti-inflammatory drugs. It has long been known that several types of antioxidants also possess analgesic and anti-inflammatory properties, indicating a strong relationship between inflammation and oxidative stress. Understanding the underlying mechanisms of action of anti-inflammatory and analgesic drugs, as well as essential targets in disease physiopathology, is essential to the development of novel therapeutic strategies. The Nuclear factor-2 erythroid related factor-2 (Nrf2) is a transcription factor that regulates cellular redox status through endogenous antioxidant systems with simultaneous anti-inflammatory activity. This review summarizes the molecular mechanisms and pharmacological actions screened that link analgesic, anti-inflammatory, natural products, and other therapies to Nrf2 as a regulatory system based on emerging evidences from experimental disease models and new clinical trial data.

BackgroundThe effect of chronic psychological stress on hepatitis and liver fibrosis is concerned. However, its mechanism remains unclear. We investigated the effect and mechanism of chronic psychological stress in promoting liver injury and fibrosis through gut.MethodsSixty male SD rats were randomly assigned to 6 groups. Rat models of chronic psychological stress (4 weeks) and liver fibrosis (8 weeks) were established. The diversity of gut microbiota in intestinal feces, permeability of intestinal mucosa, pathologies of intestinal and liver tissues, collagen fibers, protein expressions of toll-like receptor 4 (TLR4), myeloid differentiation factor 88 (MyD88), nuclear factor kappa β (NF-κβ), tumor necrosis factor α (TNF-α) and interleukin 1 (IL-1) in liver tissue, liver function and coagulation function in blood and lipopolysaccharide (LPS) in portal vein blood were detected and analyzed.ResultsThe diversities and abundances of gut microbiota were significant differences in rats among each group. The pathological lesions of intestinal and liver tissues, decreased expression of occludin protein in intestinal mucosa, deposition of collagen fibers and increased protein expression of TLR4, MyD88, NF-κβ, TNF-α and IL-1 in liver tissue, increased LPS level in portal vein blood, and abnormalities of liver function and coagulation function, were observed in rats exposed to chronic psychological stress or liver fibrosis. There were significant differences with normal rats. When the dual intervention factors of chronic psychological stress and liver fibrosis were superimposed, the above indicators were further aggravated.ConclusionChronic psychological stress promotes liver injury and fibrosis, depending on changes in the diversity of gut microbiota and increased intestinal permeability caused by psychological stress, LPS that enters liver and acts on TLR4, and active LPS-TLR4 pathway depend on MyD88. It demonstrates the possibility of existence of brain-gut-liver axis.