Anti-H1N1 influenza effects and its possible mechanism of Huanglian Xiangru Decoction.
Raktažodžiai
Santrauka
BACKGROUND
Huangliang Xiangru Decoction (HXD), which is described in a famous TCM monograph "Book of Nanyang for Life Savin", is frequently used for treating cold in summer and summer heat-dampness.
OBJECTIVE
To date, no pharmacological study on the anti-H1N1 influenza properties of HXD has been reported. The aim of the present study was to evaluate the therapeutic action of HXD on HIN1-induced acute pulmonary inflammation and its anti-influenza mechanism focus to TLRs signal pathway in a mouse model.
METHODS
the mice were intranasally infected with influenza virus to induce viral pneumonia, and then treated with different doses of HXD. The Lung index and pathological changes in the lung tissue of mice were investigated to value the anti-influenza virus effect of HXD. The concentrations of cytokines (IL-2, IL-6, TNF-α and IFN-γ) and anti-oxidant factor (NO, SOD and GSH) in serum of mice were determined with ELISA. RT-PCR and Western blot were used to determine the mRNA and protein expression of TLR3, TLR7, MyD88,TRAF3 and NF-κB p65 in the lung tissues, which are the key targets of TLRs pathway.
RESULTS
Compared with the infection group, the lung index of mice in ribavirin group, HXD high dose group and HXD middle dose group were significantly decreased, the lung indexes of these groups were 10.36±1.14mg/g, 9.89±0.79mg/g, and 10.97±0.67mg/g. Moreover, pathological changes were remarkable alleviated. HXD can reduce the contents of IL-6, TNF-α and IFN-γ, NO, and increase the contents of IL-2, SOD, GSH in serum of infected-mice significantly. At the same time, HXD can reduce the mRNA and protein expression of TLR3, TLR7, MyD88,TRAF3 and NF-κB p65 in the lung tissues of infected-mice significantly.
CONCLUSIONS
HXD has significant effects on H1N1 influenza by a quantity-effect relationship, and plays its anti-influenza effect by enhancing the body's antioxidant capacity, regulating the body's immune function and the host's TLRs pathway.
