Triptolide attenuates pressure overload-induced myocardial remodeling in mice via the inhibition of NLRP3 inflammasome expression.

Triptolide is the predominant active component of the Chinese herb Tripterygium wilfordii Hook F (TwHF) that has been widely used to treat several chronic inflammatory diseases due to its immunosuppressive, anti-inflammatory, and anti-proliferative properties. In the present study, we elucidated the cardioprotective effects of triptolide against cardiac dysfunction and myocardial remodeling in chronic pressure-overloaded hearts. Furthermore, the potential mechanisms of triptolide were investigated. For this purpose, C57/BL6 mice were anesthetized and subjected to transverse aortic constriction (TAC) or sham operation. Six weeks after the operation, all mice were randomly divided into 4 groups: sham-operated with vehicle group, TAC with vehicle group, and TAC with triptolide (20 or 100 µg/kg/day intraperitoneal injection) groups. Our data showed that the levels of NLRP3 inflammasome were significantly increased in the TAC group and were associated with increased inflammatory mediators and profibrotic factor production, resulting in myocardial fibrosis, cardiomyocyte hypertrophy, and impaired cardiac function. Triptolide treatment attenuated TAC-induced myocardial remodeling, improved cardiac diastolic and systolic function, inhibited the NLRP3 inflammasome and downstream inflammatory mediators (IL-1ß, IL-18, MCP-1, VCAM-1), activated the profibrotic TGF-ß1 pathway, and suppressed macrophage infiltration in a dose-dependent manner. Our study demonstrated that the protective effect of triptolide against pressure overload in the heart may act by inhibiting the NLRP3 inflammasome-induced inflammatory response and activating the profibrotic pathway.

[Effect of shuxuetong in preventing restenosis after intracoronary stenting].

OBJECTIVE: To evaluate the effect of shuxuetong (SXT) in preventing restenosis after intracoronary stenting. METHODS: Sixty-eight patients, accepted intracoronary stenting, were divided into two groups, the SXT group and the control group, both of them were treated with conventional treatment, and to the SXT group, SXT was given additionally. The condition of treated coronary artery restenosis in the two groups was compared by way of quantitative coronary angiography and a 6-month follow-up study was adopted. RESULTS: Follow-up study was completed in 43 patients (23 cases in the SXT group, and 20 in the control group). The angina recurrence rate in the SXT group (3 cases, 13%) was significantly lower than that in the control group (7 cases, 35%, P < 0.05). Quantitative coronary angiography showed the restenosis degree of operated artery in the SXT group was significantly milder than that in the control group, with the last lumen losing and index in the SXT group (0.46 +/- 0.25 mm, 24.26 +/- 8.64%) less than those in the control group (0.75 +/- 0.33 mm, 31.25 +/- 11.03%). The net gain lumen and the net gain index in the SXT group (1.23 +/- 0.30 mm, 58.96 +/- 24.68%) were greater than those in the control group (0.98 +/- 0.33 mm, 42.68 +/- 29.51%), all P < 0.05. But the restenosis rate in the two groups was insignificantly different (P > 0.05). CONCLUSION: SXT might has some definite effect in preventing restenosis after intracoronary stenting.