[Effects of mangiferin on MAPK signaling pathway in chronic inflammation].

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.