Literature DB >> 34093763

Toxicity of Melastoma dodecandrum Lour. and its effects on lipopolysaccharide-induced inflammation and oxidative stress.

Gang Huang1, Yuli Ge2, Zhihong Gui3, Meixiao Zhu4, Jin Liu5, Huafu Wang6.   

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.
Copyright © 2020, Spandidos Publications.

Entities:  

Keywords:  CD4+ T cell; Melastoma dodecandrum Lour; inflammation; mitochondrial apoptosis; oxidative stress

Year:  2021        PMID: 34093763      PMCID: PMC8170668          DOI: 10.3892/etm.2021.10239

Source DB:  PubMed          Journal:  Exp Ther Med        ISSN: 1792-0981            Impact factor:   2.447


  24 in total

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