[Effect of Triptolide on Cardiac Function in Arthritic Rats and Its Mechanism].

OBJECTIVE

To observe the changes of cardiac function in arthritic rats and the effect of triptolide on it.

METHODS

Forty rats were divided in random into normal control (NC) group, model control (MC) group, leflunomide (LEF) group and triptolide (TP) group. Except for the normal group, rats in the other three groups were injected with Freund's complete adjuvant to create arthritic inflammation in the right hind paws, and the interventional drug was administered on the 12th day after the inflammation. By treating for 30 d, the cardiac function of rats was detected by left ventricular catheterization. The expressions of superoxide dismutase (SOD), malondialdehyde (MDA), reacitve oxygen species (ROS), total antioxidation (T-AOC), interleukin-10 (IL-10) and tumor necrosis factor-α (TNF-α) in serum were measured by enzyme-linked immunosorbent assay. The expressions of keap-like protein 1 ( 1), muscular aponeurotic fibrosarcom ( ) and nuclear factor-E2 related factor2 ( 2) mRNAs in cardiac tissue were detected by real-time PCR. The expressions of Keap1, maf and Nrf2 proteins in heart tissues were detected by Western blot.

RESULTS

Comparing with the normal group, the heart rate (HR), heart index (HI), left ventricular systolic pressure (LVSP), and left ventricular end-diastolic pressure (LVEDP) of the model group were significantly increased, whereas the maximum change rate of ventricular pressure rise or decline (±dp/dtmax) was significantly decreased ( <0.01). SOD, MDA, ROS, T-AOC, and TNF-α were all increased, and IL-10 was significantly decreased ( <0.01). The mRNA and protein expressions of Keap1, maf and Nrf2 in heart tissues were increased ( <0.01). Comparing with the model group, HR, HI, LVSP, and LVEDP in the triptolide group were significantly decreased, whereas the ±dp/dtmax was significantly increased ( <0.01). SOD, MDA, T-AOC, ROS, TNF-α decreased while the IL-10 increased ( <0.05, <0.01). The expressions of 1, and 2 mRNAs and proteins in the heart tissues of the triptolide group were decreased ( <0.01).

CONCLUSION

Triptolide could improve cardiac function in arthritic rats, and the mechanism may related to its ability of improving the anti-oxidationin cardiomyocytes, reducing oxidative stress damage, and inhibiting abnormal immune inflammatory response.