Rumex crispus Leaf Extract Inhibits Lipopolysaccharide-Induced Inflammatory Response in BV-2 Microglia Cells

被引:1
|
作者
Park, Ji-Woong [1 ,2 ,3 ]
Kim, Woong [3 ,4 ]
Choi, Chul Yung [1 ,2 ,3 ,4 ]
Kim, Seok-Jun [1 ,2 ,3 ,4 ,5 ]
机构
[1] Chosun Univ, Dept Integrat Biol Sci, Gwangju 61452, South Korea
[2] Chosun Univ, BK21 FOUR Educ Res Grp Age Associated Disorder Co, Gwangju 61452, South Korea
[3] Chosun Univ, Inst Well Aging Medicare, Gwangju 61452, South Korea
[4] Chosun Univ, Dept Biomed Sci, Gwangju 61452, South Korea
[5] Chosun Univ, Gwangju Alzheimers & Related Dementia Cohort Res, Gwangju 61425, South Korea
关键词
Rumex crispus; neuroinflammation; microglia; cytokine; MAPK/NF-kappa B pathway; NF-KAPPA-B; NITRIC-OXIDE; CYTOKINES; MAPK; NEUROINFLAMMATION; RESVERATROL; ANTIOXIDANT; QUERCETIN; FLAVONES; L;
D O I
10.3390/pr11092756
中图分类号
TQ [化学工业];
学科分类号
0817 ;
摘要
Background: Microglial cells are immune cells that operate within the central nervous system. Abnormally activated microglia cause neuroinflammation, which is linked with neurodegenerative disease. Previous research has revealed that Rumex crispus root extract exerts anti-inflammatory effects. However, it is not known whether Rumex crispus leaf extract (RLE) has anti-inflammatory effects on murine microglial cells, such as BV-2 cells. This study proposed to investigate the impact of RLE on inducing inflammation by LPS in BV-2 cells. Methods: LPS was used to induce inflammation in BV-2 cells, and then cell survival, changes in the levels of inflammation-related factors and pro-inflammatory cytokines, and NF-kappa B and MAPKs signaling pathway activity were evaluated in the presence or absence of RLE. Results: RLE treatment resulted in a reduction in nitric oxide (NO) production triggered by LPS without causing cytotoxic effects. In addition, both protein and mRNA expression levels of iNOS and COX-2, which were upregulated by LPS, were significantly decreased by RLE. Also, RLE effectively reduced the transcriptional expression and further suppressed the increased production of inflammatory cytokines by LPS stimulation. Additionally, RLE effectively suppressed the inflammatory response of BV-2 cells stimulated by LPS via interference with NF-kappa B and MAPK signaling pathways. Conclusions: Taken together, our results confirm the effective suppression of the inflammatory response induced by LPS in BV-2 cells by RLE. Consequently, we suggest that RLE holds promise as a preventive agent against diseases triggered by microglial inflammatory responses.
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页数:11
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