Myricetin attenuated LPS induced cardiac injury in vivo and in vitro

Abstract

Sepsis induced myocardial dysfunction (SIMD) is a common complication and leads to an increased mortality. SIMD is closely related to inflammation and oxidative stress. Myricetin exhibits strong capacities of anti-inflammation and anti-oxidative stress, but its pharmacological effects for lipopolysaccharide (LPS) induced cardiac injury remains undefined. This study aimed to explore whether myricetin was efficient to alleviate SIMD in mice and neonatal rat cardiomyocytes injury. Mice administrated with myricetin (100 mg/kg, po, bid) or vehicle groups were challenged with LPS (10 mg/kg, ip), and cardiac functions examined by echocardiography after 12 hr LPS exposure. LPS markedly impaired mouse cardiac functions, which were significantly attenuated by myricetin administration. Myricetin significantly reduced the production of inflammatory cytokines both in serum and cardiac tissue. Myricetin could inhibit the nuclear translocation of p65, degradation of IκBα, and cellular apoptosis in vivo and in vitro. Myricetin also prevented overexpression of iNOS and reduction of oxidoreductase (SOD and GPx) activity. Besides, Myricetin treatment could attenuate production of inflammatory cytokines of peritoneal macrophages stimulated with LPS in vitro. Thus we concluded that myricetin could attenuate the LPS induced cardiac inflammation injury in vivo and in vitro. Myricetin may be a potential therapy or adjuvant therapy for SIMD.

RETRACTED ARTICLE: Protective functions of myricetin in LPS-induced cardiomyocytes H9c2 cells injury by regulation of MALAT1

“…In the present study, we found a significantly prohibitive function of myricetin on the phosphorylated expression of p65 and IκBα. Our results appeared to be consistent with a previous study that myricetin significantly attenuated LPS-induced IκB degradation, and nuclear translocation of p65 and NF-κB DNA-binding activity in LPS-treated macrophages [17, 28]. Accordingly, the expression of cytokines is regulated.…”

“…We found that myricetin exhibited pro-proliferative and anti-apoptotic effects in LPS-induced inflammatory injury of cardiomyocytes. Analogously, its cardio-protective function has been proved in ischemia/reperfusion rat model and sepsis-induced myocardial dysfunction mice model [17, 21], while a few epidemiological and clinical findings have been reported in the benefits of myricetin on myocarditis. Most probably, it is due to its poor water solubility and oral bioavailability that hinder its potential use [22].…”

“…In addition, it also has been proved to suppress inflammation in several models [15, 16]. Although a few clinical studies have been conducted, the cardio-protective effects of myricetin against inflammatory injury have recently been validated in vivo and in vitro [17, 18]. As a consequence, the preservation of myocardial anti-inflammatory capacity and the inhibition of inflammation-elicited lesions by application of myricetin are an appealing approach against myocarditis.…”

Resveratrol Inhibits Ischemia-Induced Myocardial Senescence Signals and NLRP3 Inflammasome Activation

“…Peritoneal macrophages were prepared in our laboratory from adult C57/B6 male mice according to our previously reported methods [ 17 ]. Macrophages were cultured in RPMI 160 culture medium containing 15% heat inactivated fetal bovine serum for 1 h. The supernatant was removed, and the adherent cells were peritoneal macrophages.…”

Current Pharmacological Trends on Myricetin

“…Myricetin also prevented over expression of induced nitric oxide synthase (iNOS) and reduction of oxidoreductase (SOD and GPx) activity. Besides, Myricetin treatment could attenuate production of inflammatory cytokines of peritoneal macrophages stimulated with LPS in vitro [55].…”