MECHANISM OF GINSENOSIDE IN THE TREATMENT OF HEART FAILURE BY INTERVENING PPAR PATHWAY

Yuhong Zhao, Bin Wu, Lei Yan, Hualing Lu, Lijun Zhu, Weiran Tian, Qiayi Ma, Yan Li^*

Department of internal medicine, Shanghai Changning Tianshan Traditional Chinese Medicine Hospital, Shanghai 200050, China

Objective: To analyze the therapeutic effect and related mechanism of ginsenoside on heart failure. 

Methods: A total of sixty male SD rats were randomly allocated to a control group, a model group and a drug group. The rats in the control group were not treated. The rats in the model group and the drug group were treated to establish a heart failure model. The rats in the model group were also given the total ginsenoside gavage treatment, and the heart function of the rats was analyzed using color Doppler ultrasound after treatment. The heart mass index of each group was calculated and serum levels of BNP, ATP and ADP were measured by ELISA. Western blot assay was used to determine levels of mitogen activated protease p38 (p38MAPK), phosphorylated mitogen activated protease p38 (P-P38MAPK), and peroxisome proliferator activated receptor (PRR) in rats of each group. Bcl-2 and Bax protein content was studied. 

Results: LVDD and LVDS levels in the model group were significantly higher than those in the control group, and levels of LVEF, LVPWD and LVPWS in the model group were significantly lower than those in the control group. LVDD and LVDS levels in the drug group were significantly lower than those in the model group, and levels of LVEF, LVPWD and LVPWS in the drug group were significantly higher than those in the model group (P<0.05). The heart mass index of the model group was significantly higher than that of the control group, and the heart mass index of the drug group was significantly lower than that of the model group (P<0.05). Levels of BNP and ADP in the model group were significantly higher than those in the control group, and the ATP level in the model group was significantly lower than it was in the control group. Levels of BNP and ADP in the drug group were significantly lower than those in the model group, and the ATP level in the drug group was significantly higher than it was in the model group (P<0.05). Bax level in the model group was significantly higher than that in the control group, and Bcl-2 level was significantly lower than that in the control group. The Bax level of the rats in the drug group was significantly lower than that in the model group, and the level of Bcl-2 in the drug group was significantly higher than that in the model group (P<0.05). Levels of p38MAPK and P-P38MAPK in the model group were significantly higher than those in the control group. The PPAR- γ level in the model group was significantly lower than that in the control group. Levels of p38MAPK and P-P38MAPK in the drug group were significantly lower than those in the model group. The PPAR- γ level of the drug group was significantly higher than that of the model group (P<0.05). 

Conclusion: Ginsenoside can delay the development of heart failure in rats with heart failure. The mechanism may be related to the regulation of PPAR pathway related proteins by ginsenoside.