Protective effects and mechanism of curcumin on myocardial injury induced by coronary microembolization

Abstract

Objective Coronary microembolization (CME) is a common complication during the percutaneous coronary intervention (PCI). CME‐induced local myocardial inflammation and myocardial apoptosis are the primary causes of progressive cardiac dysfunction. Curcumin exerts a protective role in various cardiovascular diseases; however, its effects in CME are yet to be clarified. Therefore, the current study investigated the effects of curcumin on myocardial inflammatory responses, myocardial apoptosis, and cardiac dysfunctions induced by CME in rats. Methods A total of 40 Sprague–Dawley rats were randomly divided into the following groups: Sham operation (sham group), CME group, curcumin, and control with 10 rats in each group. The ascending aortas were clamped, and the CME‐model group was established by injecting microspheres into the apex of the left ventricle. An equivalent amount of normal saline was injected to establish the sham group. The cardiac functions, serum c‐troponin I level, and apoptotic index was examined. Also, the levels of Toll‐like receptor 4 (TLR4), myeloid differentiation primary response 88 (MYD88), nuclear factor κB (NF‐κB) p65, BCL2‐associated X protein (Bax), B‐cell lymphoma 2 (Bcl‐2), cleaved caspase‐3, tumor necrosis factor α (TNF‐α), and interleukin‐1β (IL‐1β) were detected. Results Myocardial dysfunction enhanced serum c‐troponin I, and apoptotic index were induced following CME. Moreover, CME elevated the expression of TLR4, MyD88, NF‐κB p65, cleaved caspase‐3, TNF‐α, and IL‐1β, while the Bcl‐2/Bax ratio decreased. Curcumin reversed these effects by CME, while the gastric lavage control did not exert any effect. Conclusion Curcumin was responsible for the anti‐CME‐induced myocardial injury. The effector mechanism might be related to the reduction of cardiomyocyte apoptosis and inhibition of myocardial inflammatory responses mediated by TLR4/MyD88/NF‐κB signaling pathway.

Curcumin Nanoparticles Versus Curcumin in Amelioration of Inflammatory and Pathological Changes During the Migratory Phase of Murine Trichinellosis

“…tween serum Trop & cardiac expression of caspase 3. This agreed with Yeh et al (2005)andLiu et al (2017) Liu et al (2019). found that Cur effectively reduced myocardial injury, inhibited myocardial apoptosis and improved cardiac functions.…”

The Guizhi Gancao Decoction Attenuates Myocardial Ischemia-Reperfusion Injury by Suppressing Inflammation and Cardiomyocyte Apoptosis

“…This is consistent with the belief that besides its role in innate immune responses, TLR4 serves as a proinflammatory agent in murine myocardial I/R injury. Also, studies have exhibited that the effect of TLR4- mediated inflammatory response in I/R injury was related to activation of NF- κ B and other proinflammatory cytokines including TNF- α and IL-1 β [39, 40]. RC and RG have been shown to effectively inhibit proinflammatory cytokine production because of their immunomodulatory effects [19–21].…”

Breviscapine Pretreatment Inhibits Myocardial Inflammation and Apoptosis in Rats After Coronary Microembolization by Activating the PI3K/Akt/GSK-3β Signaling Pathway

“…Therefore, inhibition of myocardial inflammation and apoptosis can distinctly improve cardiac function and myocardial injury. 3,4 Moreover, studies by Liang et al 5 and Kong et al 6 demonstrated that myocardial apoptosis and inflammation can induce heart dysfunction and myocardial injury, after CME in rats. However, pretreatment with ligustrazine significantly reduced myocardial apoptosis and inflammation induced by CME, thus relieving myocardial injury and ameliorating cardiac contractile function by activating the phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt) pathway.…”