Cardioprotective effects of rhamnetin in H9c2 cardiomyoblast cells under H2O2-induced apoptosis

Kaempferol protects cardiomyocytes against anoxia/reoxygenation injury via mitochondrial pathway mediated by SIRT1

“…The study of SIRT1, 2 and 3 is a hot spot of current research. Previous experiments showed that the up-regulation of SIRT1 and SIRT3 or down-regulation of SIRT2 can attenuate cell apoptosis (Kume et al, 2006;Pang et al, 2013;Park et al, 2014;Lynn et al, 2008). SIRT1 is shown to deacetylate many non-histone proteins including p53, Foxo and PPARγ that are known to play a crucial role in cell survival, metabolism and stress response (Li et al, 2007;Motta et al, 2004;Tanno et al, 2007;Vaziri et al, 2001).…”

The Protective Effect of INH₂BP, a Novel PARP Inhibitor 5-Iodo-6-Amino-1,2-Benzopyrone, Against Hydrogen Peroxide-Induced Apoptosis Through ERK and p38 MAPK in H9c2 Cells

“…Cardiovascular disorders are linked to generate the elevated H 2 O 2 from damaged cells, which reported the primary cause of pathogenesis as well as apoptosis of cardiomyocyte [23] . Therefore, we previously suggested that the suppression of cardiomyocyte apoptosis against excessive ROS is a major therapy goal [7] . Recently, an experimental evidence of the improved cardiac function was implicated by INO-1001 as well as PARP inhibitor, whereas the ROS-induced PARP activation led to the cell death [24, lar functions such as the proliferation and migration in diverse cells, regulation of cancer growth and protection of cardiomyocytes apoptosis [43,44] .…”

“…Chen et al [3] showed that ROS may affect intercellular connections and cytoskeleton resulting in cell detachment, morphology change, or death. Excess ROS causes cell damage that regulates signal transduction-related proteins by phosphorylating or modifying the active sites of proteins but also inhibits phosphatase activity [7] . Blocking the excess ROS production has been suggested to constitute a promising therapeutic approach for the treatment of cardiovascular diseases including cardiac hypertrophy [8] .…”

“…Diverse studies have shown that ROS can encourage cellular functions such as cell proliferation, migration, death and apoptosis [26,27] . In particular, excessive ROS production possibly promotes human disorders [7,28] . Despite the fact that superoxide anion disarranged the stabilized state of heart which is one of the leading causes of cardiovascular disease, the superoxide scavenging enzymes such as Mn-SOD and Zn-SOD exert to maintain redox homeostasis [29,30] .…”

Carbocisteine attenuates hydrogen peroxide-induced inflammatory injury in A549 cells via NF-κB and ERK1/2 MAPK pathways

“…Mitogen activated protein kinases (MAPKs) are evolutionarily conserved mediators in signal transduction pathways, which modulate embryogenesis, gene expression and cell functions [6]. The target genes of NF-κB and MAPK signal pathways include cytokines and chemokines, such as IL-1β, IL-6, IL-8, TNF-α, MCP-1, IP-10 and MIP.…”