No abstract

Melastoma dodecandrum Lour. (MDL) is component used in traditional Chinese medicine that is widely distributed throughout southern China. MDL has been long utilized in clinical treatment for various conditions, such as inflammation. However, the toxicity and underlying anti-inflammatory mechanism of MDL remain to be elucidated. In the present study, Sprague-Dawley rats received intragastric administration of MDL for 2 months, and the toxicity of MDL was investigated. The rats were treated with lipopolysaccharide (LPS) for 8 h to determine the potential anti-inflammatory mechanism of MDL. The results demonstrated that MDL alone did not affect the expression levels of factors associated with inflammation (IL-1β, IL-6 and TNF-α) and oxidative stress [malondialdehyde (MDA), superoxide dismutase (SOD) and nitric oxide (NO)] in the rat serum and exerted no effects on rat liver and kidneys. By contrast, MDL attenuated LPS-induced inflammation and oxidative stress by regulating specific cytokines, such as IL-1β, IL-6, TNF-α, MDA, SOD and NO in the rat serum and alleviated LPS-induced liver and kidney damage. Additionally, compared with the LPS group, MDL inhibited CD4 + T cell differentiation into Th1 and Th17 cells and enhanced CD4 + T cell differentiation into Th2 and Treg cells. MDL also suppressed reactive oxygen species (ROS) production and mitochondrial apoptosis by modulating mitochondrial apoptosis-related proteins in spleen CD4 + T cells. In conclusion, the results of the present study demonstrated the non-toxic nature of MDL and revealed that it alleviated LPS-induced inflammation and oxidative stress by regulating differentiation and ROS production in CD4 + T cells.

No abstract

Alcoholic liver disease (ALD) is a common clinical liver injury disease. Lactobacillus rhamnosus Gorbach-Goldin (LGG) has been revealed to alleviate alcohol-induced intestinal barrier and liver injury. However, the underlying mechanism of LGG treatment for ALD remains unclear. To clarify this aspect, a chronic plus binge ALD model was constructed using C57BL/6 mice in line with a chronic alcohol binge feeding protocol. Interleukin 22 (IL-22) level was determined by quantitative real-time polymerase-chain reaction and enzyme-linked immunosorbent assays. Effects of LGG in model or IL-22 knockdown in LGG-treated model on the liver injury and steatosis status, as well as intestinal barrier function were assessed by hematoxylin eosin (HE) staining. Levels of alanine aminotransferase (ALT), triglyceride (TG), and aspartate aminotransferase (AST) in serum were measured by the corresponding kit. Western blot analysis was conducted to detect protein expressions of intestinal tight junction protein 1 (ZO-1) and Claudin-1. Concretely, LGG elevated IL-22 level in liver tissues and serum, while inhibiting ALT, TG, and AST levels in alcohol-exposed mice. Moreover, LGG alleviated liver injury, steatosis, and intestinal barrier injury caused by alcohol, and enhanced ZO-1 and Claudin-1 expressions. Furthermore, IL-22 knockdown increased ALT, TG, and AST levels in serum, and aggravated liver injury, steatosis, and intestinal barrier injury. ZO-1 and Claudin-1 levels were downregulated by IL-22 silencing. Importantly, downregulation of IL-22 reversed the effect of LGG on the liver and intestinal barrier injury. To conclude, LGG protects against chronic alcohol-induced intestinal and liver injury via regulating the intestinal IL-22 signaling pathway.

No abstract