Astragaloside IV prevents lipopolysaccharide-induced injury in H9C2 cardiomyocytes

This study aimed to investigate the protective effects of astragaloside IV(AS IV) on lipopolysaccharide(LPS)-induced injury in H9C2 cardiomyocytes. H9C2 Cardiomyocytes were cultured with LPS(10 μg·mL-1) for 4 h and treated with AS IV at 50, 100, and 150 μmol·L-1 for various durations. Cell viability was determined by MTT. The content of released TNF-α and IL-6 from cardiomyocytes were evaluated by enzyme-linked immunosorbent assay(ELISA). The levels of superoxidase dismutase(SOD), malondialdehyde(MDA), lactate dehydrogenase(LDH), and creatine phosphate kinase(CK) were measured by using commercial available kits. The mR NA and protein expression levels of NF-κB p65 were measured by RT-PCR and Western blotting, respectively. And the NF-κB p65 activity was measured by ELISA. Our results demonstrated that AS IV at 50, 100, and 150 μmol·L-1 markedly inhibited the release of TNF-α and IL-6 and decreased NF-κB expression, compared with the model group. Moreover, the improved SOD activity and decreased MDA, LDH and CK levels were detected after AS IV treatment. In summary, AS IV could increase the activities of antioxidant enzymes, inhibite lipid peroxidation, and down-regulate the inflammatory mediators involved in the inflammatory responses. These results demonstrated that AS IV could prevent LPS-induced injury in cardiomyocytes.

Chlorogenic acid ameliorates heart failure by attenuating cardiomyocyte ferroptosis Author links open overlay panel

Objective To elucidate the effects of chlorogenic acid(CGA),a bioactive polyphenol compound prevalent in traditional Chinese medicine and various foods,including Lonicera japonica Thunb.(Jin Yin Hua),Eucommia ulmoides Oliv.(Du Zhong Ye),tea,and coffee,on cardiomyocyte ferroptosis and heart failure.Methods We assessed the effect of CGA on cardiac function using a mouse model of heart failure induced by transverse aortic constriction(TAC).These indicators included the left ventricular ejection fraction(LVEF),fractional shortening(LVFS),end-systolic volume(LVESV),end-diastolic volume(LVEDV),end-systolic diameter(LVESD),and end-diastolic diameter(LVEDD).An isoprenaline hydrochloride(ISO)-induced H9c2 cardiomyocyte cell model was also established,and the cells were treated with various concentrations of CGA.To assess the effect of CGA on ferroptosis in cardiomyocytes,we measured cell viability and evaluated the levels of intracellular reactive oxygen species(ROS),ferrous ions(Fe^(2+)),and lipid peroxidation using fluorescent staining.To clarify the ferroptosis signaling pathway regulated by CGA,western blotting was used to examine the expression of ferroptosis biomarkers,specifically solute carrier family 7 member 11(SLC7A11)and glutathione peroxidase 4(GPX4),in H9c2 cardiomyocytes and mouse myocardial tissues.Results CGA significantly enhanced cardiac performance indices such as LVEF,LVFS,LVESV,LVEDV,LVESD,and LVEDD.H9c2 cardiomyocytes exposed to ISO showed decreased cell viability and increased ROS levels,Fe^(2+)content,and lipid peroxidation levels.However,CGA treatment significantly ameliorated these changes.Additionally,in both H9c2 cardiomyocytes and myocardial tissue obtained from mice with TAC,CGA increased the expression of ferroptosis-related proteins,including SLC7A11 and GPX4.Conclusion CGA has the potential to enhance cardiac function and diminish lipid peroxidation and ROS levels in cardiomyocytes via the SLC7A11/GPX4 signaling pathway.This process alleviates ferroptosis in cardiomyocytes.These results provide new insights into the clinical use of CGA and the management of heart failure.

Hydrogen sulfide protects against high glucose-induced H9c2 cardiomyocyte injury and inflammatory response by inhibiting ROS-TLR4 pathway

Objective To investigate whether exogenous hydrogen sulfide（H2S）protects high glucose（HG）-inducedH9c2 cardiomyocyte injury and inflammation response by inhibiting reactive oxygen species（ROS）-Toll-like receptor 4（TLR4）pathway.Methods Cell counter kit-8（CCK-8）assay was used to measure the cell viability,