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[Effects of mangiferin on MAPK signaling pathway in chronic inflammation]
Zhiquan Wei1, Li Yan, Jiagang Deng
1Guangxi Medical University, Nanning 530021, China.
Objective:
To investigate mechanism of inhibition on the lipopolysaccharide induced chronic inflammation of mangiferin by the regulation of mitogen-activated protein kinase (MAPK) signaling pathway.
Method:
Sixty SD rats were randomly divided into normal control, model control, positive drug control (prednisone, 5 mg x kg(-10 x d(-1)) and mangiferin (200, 100, 50 mg x kg(-1) x d(-1)) group. The chronic inflammation models were established by intermittent injection of lipopolysaccharide via the tail vein. The leucocyte count was measured. The levels of serum tumor necrosis factor alpha (TNF-alpha), interleukin-6 (IL-6) and soluble intercellular adhesion molecule 1 (sICAM-1) were detected by enzyme-linked immunosorbent assay (ELISA). The reverse transcription-polymerase chain reaction (RT-PCR) was applied to evaluate the expressions of p38, ERK, JNK gene of leucocyte in MAPK signaling pathway.
Result:
Compared with the model control, not only the leucocyte count and the level of serum TNF-alpha, IL-6, sICAM-1 but also the expressions of ERK, JNK gene of leukocyte were markedly reduced in mangiferin (200 mg x kg(-1) x d(-1)) group (P < 0.05). However, there was no statistics significance for the expression of p38 gene between the model control and the mangiferin (200 mg x kg(-1) x d(-1)) group.
Conclusion:
As a possible mechanism, the regulation of mangiferin on the expressions of ERK, JNK gene of leukocyte in MAPK signaling pathway was involved in its great inhibition on the chronic inflammation induced by lipopolysaccharide.
Insights
Mangiferin effectively inhibits chronic inflammation by downregulating ERK and JNK genes within the mitogen-activated protein kinase (MAPK) pathway. This study reveals mangiferin
Area of Science:
- Pharmacology
- Immunology
- Molecular Biology
Context:
- Chronic inflammation is a significant health concern.
- Lipopolysaccharide (LPS) is a potent inducer of inflammation.
- The mitogen-activated protein kinase (MAPK) pathway plays a critical role in inflammatory responses.
Purpose:
- To elucidate the anti-inflammatory mechanism of mangiferin.
- To investigate mangiferin's effect on the MAPK signaling pathway in LPS-induced chronic inflammation.
Summary:
- Mangiferin treatment significantly reduced leukocyte count and serum levels of TNF-alpha, IL-6, and sICAM-1 in rats with chronic inflammation.
- Mangiferin markedly downregulated the expression of ERK and JNK genes in leukocytes.
- No significant effect was observed on p38 gene expression.
Impact:
- Mangiferin demonstrates potential as a therapeutic agent for chronic inflammatory conditions.
- The findings highlight the role of MAPK pathway regulation in mangiferin's anti-inflammatory effects.
- This research provides a mechanistic basis for mangiferin's use in managing LPS-induced inflammation.
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