OBJECTIVE: To investigate effects of Xinfeng capsule (XFC) on cardiac function in rats with adjuvant arthritis (AA) and explore the mechanism of these effects. METHODS: Forty-eight rats were randomly divided into normal control (NC), model control (MC), methotrexate (MTX) and XFC groups of equal size. In all groups except for the NC group, 0.1 mL Freund's complete adjuvant (FCA) was intracutaneously injected in the right rear vola pedis to induce inflammation. Drugs were applied beginning 19 days after induction of inflammation. Normal saline was administered to the NC and MC groups and 1 mg/ 100 g MTX (weekly) and 0.12 g/100 g XFC (daily) to the MTX and XFC groups, respectively. Rats were sacrificed after 30 day of treatment. Toe swelling degree (TSD), arthritis index (Al), cardiac function and expression of nuclear factor kappa B (NF-κB)/tumor necrosis factor alpha (TNF-α) and transforming growth factor beta 1 (TGF-β1)/Smads pathway proteins were measured. RESULTS: In the MC group, TSD and Al were greatly increased, while parameters of cardiac function were decreased and morphological analysis showed myocardial cell damage. Expression of TNF-α, NF-KB, Smad2, P-Smad2, Smad4 and TGF-β1 proteins were elevated in cardiac tissue, while Smad7 expression was decreased. TSD and Al values closely correlated to parameters of cardiac function and to levels of proteins in the NF-κB/TNF-α and TGF-β1/Smads pathways. Certain correlations were identified among TGF-β1 and NF-KB, Smad2, P-Smad2 and Smad4. With XFC intervention, both TSD and Al were decreased and parameters of cardiac function and ultrastructure of myocardial cells improved. Expressions of NF-κB, Smad2, and Smad4 proteins were greatly decreased and Smad7 expression was elevated, as compared with levels in the MC and MTX groups. CONCLUSION: XFC regulates expression of proteins in the NF-KB/TNF-α and TGF-β1/Smads pathways, decreases immune complex deposition in cardiac tissue and improves cardiac function in AA rats via upregulation of Smad7.
OBJECTIVE: To investigate effects of Xinfeng capsule (XFC) on cardiac function in rats with adjuvant arthritis (AA) and explore the mechanism of these effects. METHODS: Forty-eight rats were randomly divided into normal control (NC), model control (MC), methotrexate (MTX) and XFC groups of equal size. In all groups except for the NC group, 0.1 mL Freund's complete adjuvant (FCA) was intracutaneously injected in the right rear vola pedis to induce inflammation. Drugs were applied beginning 19 days after induction of inflammation. Normal saline was administered to the NC and MC groups and 1 mg/ 100 g MTX (weekly) and 0.12 g/100 g XFC (daily) to the MTX and XFC groups, respectively. Rats were sacrificed after 30 day of treatment. Toe swelling degree (TSD), arthritis index (Al), cardiac function and expression of nuclear factor kappa B (NF-κB)/tumor necrosis factor alpha (TNF-α) and transforming growth factor beta 1 (TGF-β1)/Smads pathway proteins were measured. RESULTS: In the MC group, TSD and Al were greatly increased, while parameters of cardiac function were decreased and morphological analysis showed myocardial cell damage. Expression of TNF-α, NF-KB, Smad2, P-Smad2, Smad4 and TGF-β1 proteins were elevated in cardiac tissue, while Smad7 expression was decreased. TSD and Al values closely correlated to parameters of cardiac function and to levels of proteins in the NF-κB/TNF-α and TGF-β1/Smads pathways. Certain correlations were identified among TGF-β1 and NF-KB, Smad2, P-Smad2 and Smad4. With XFC intervention, both TSD and Al were decreased and parameters of cardiac function and ultrastructure of myocardial cells improved. Expressions of NF-κB, Smad2, and Smad4 proteins were greatly decreased and Smad7 expression was elevated, as compared with levels in the MC and MTX groups. CONCLUSION: XFC regulates expression of proteins in the NF-KB/TNF-α and TGF-β1/Smads pathways, decreases immune complex deposition in cardiac tissue and improves cardiac function in AA rats via upregulation of Smad7.