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

Exp Ther Med. 2021 Aug;22(2):807. doi: 10.3892/etm.2021.10239. Epub 2021 May 27.

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.

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

Grants and funding

Funding: This work was supported by the Lishui Science and Technology Planning Project (grant no. 2016zdyf02), the Zhejiang Pharmaceutical Association Hospital Pharmaceutical Research Project (grant no. 2016ZYY40) and The Lishui High-level Talent Fund Project (grant no. 2017RC19).