OBJECTIVETo observe the effects of Xinfeng Capsule (XC) on the cardiac function and the myocardial ultrastructure in rats with adjuvant arthritis (AA).

METHODSSixty rats were randomly divided into the normal control group, the model group, the methotrexate (MTX) treated group, the Tripterygium Glycosides Tablet (TGT) treated group, and the XC treated group, 12 in each group. Except those in the normal control group, rats in the rest groups were induced to establish the AA model by intradermally injecting Freund's complete adjuvant into their right paws. The medication was started from the 19th day. Normal saline was administered to rats in the normal control group and the model group. MTX, TGT, and XC was respectively administered to rats in the MTX, TGT, and XC groups. The medication lasted for 30 days. The swelling degree of voix pedis, arthritis index (AI), the heart function, serum levels of cytokines, and the myocardial ultrastructure were observed.

RESULTS(1) Compared with the normal control group, the swelling degree of voix pedis and AI significantly increased (P < 0.01), the body weight significantly decreased (P < 0.05) in the model group and the other 3 treated groups. (2) Compared with the model group, the heart index (HI), left ventricular systolic pressure (LVSP), and left ventricular end diastolic pressure (LVEDP) significantly decreased (P < 0.05, P < 0.01), the maximum rate of left ventricular pressure of development or decline (+/- dp/dt(max)) significantly increased (P < 0.05, P < 0.01). Compared with the MTX treated group, the LVSP and LVEDP significantly decreased (P < 0.05), and +/- dp/dtmax significantly increased (P < 0.05). (3) Compared with the model group, TNF-alpha, brain natriuretic peptide (BNP), and IL-17 significantly decreased (P < 0.05, P < 0.01); IL-10, CD4+, CD4+ CDA25+ significantly increased (P < 0.05, P < 0.01). Compared with the MTX treated group, IL-17 significantly decreased (P < 0.05), CD4+ CD25+ expression significantly increased in the XC group (P < 0.05). (4) Transmission electron microscopy showed that myocardial ultrastructure was basically contact in the XC treated group, approaching to that of the normal control group.

CONCLUSIONSDecreased cardiac function and damaged myocardial ultrastructure existed in AA rats. XFC could ameliorate the swelling degree of voix pedis and AI, as well as improve the heart function. Its mechanisms might be correlated with down-regulating serum levels of inflammatory factors, up-regulating the expressions of anti-inflammation factors, thus improving the myocardial ultrastructure and protecting injured myocardial cells.