Search

Kaempferol has been demonstrated to provide benefits for the treatment of atherosclerosis, coronary heart disease, hyperlipidemia, and diabetes through its antioxidant and anti-inflammatory properties. However, its role in cardiac hypertrophy remains to be elucidated. The aim of our study was to investigate the effects of kaempferol on cardiac hypertrophy and the underlying mechanism. Mice subjected to aorta banding were treated with or without kaempferol (100mg/ kg/d, p. o.) for 6 weeks. Echocardiography was performed to evaluate cardiac function. Mice hearts were collected for pathological observation and molecular mechanism investigation. H9c2 cardiomyocytes were stimulated with or without phenylephrine for in vitro study. Kaempferol significantly attenuated cardiac hypertrophy induced by aorta banding as evidenced by decreased cardiomyocyte areas and interstitial fibrosis, accompanied with improved cardiac functions and decreased apoptosis. The ASK1/MAPK signaling pathways (JNK1/2 and p38) were markedly activated in the aorta banding mouse heart but inhibited by kaempferol treatment. In in vitro experiments, kaempferol also inhibited the activity of ASK1/JNK1/2/p38 signaling pathway and the enlargement of H9c2 cardiomyocytes. Furthermore, our study revealed that kaempferol could protect the mouse heart and H9c2 cells from pathological oxidative stress. Our investigation indicated that treatment with kaempferol protects against cardiac hypertrophy, and its cardioprotection may be partially explained by the inhibition of the ASK1/MAPK signaling pathway and the regulation of oxidative stress. [ABSTRACT FROM AUTHOR]

Mitogen-activated protein kinase (MAPK) signaling pathways play an essential role in the transduction of environmental stimuli to the nucleus, thereby regulating a variety of cellular processes, including cell proliferation, differentiation and programmed cell death. The components of the MAPK extracellular activated protein kinase (ERK) cascade represent attractive targets for cancer therapy as their aberrant activation is a frequent event among highly prevalent human cancers. MAPK networks are a model for computational simulation, mostly using ordinary and partial differential equations. Key results showed that these networks can have switch-like behavior, bistability and oscillations. In this work, we consider three representative ERK networks, one with a negative feedback loop, which present a binomial steady state ideal under mass-action kinetics. We therefore apply the theoretical result present in [27] to find a set of rate constants that allow two significantly different stable steady states in the same stoichiometric compatibility class for each network. Our approach makes it possible to study certain aspects of the system, such as multistationarity, without relying on simulation, since we do not assume a priori any constant but the topology of the network. As the performed analysis is general it could be applied to many other important biochemical networks. [ABSTRACT FROM AUTHOR]

Describes the new findings in ischemia&nfrsl;reperfusion research from investigators in the U.S., Italy and South Africa. Inducement of apoptosis by protein kinase C-delta activation in response to cardiac ischemia and reperfusion damage; Prevention of oxidative myocardial injury induced by ischemia and reperfusion caused by oleuropein; Regulatory functions of p38 and JNK on the development of apoptosis during simulated ischemia and reperfusion.

Investigates the inhibition of MAPK signaling pathways by Vibrio outer protein A from Vibrio parahaemolyticus. Details on the causative agent of gastroenteritis endemic; Insight into the immense activity of targets utilized by YopJ-like effectors; Survival of host cell during infection.

Reports on the link between stress-activated MAPK and cAMP-dependent protein kinase pathways via a chromatin modeling. Importance of interaction between different signal transduction pathways for developmental decisions; Effect of direct interpathway connection co-ordinated signals of nitrogen and carbon source depletion on g[0] cell-cycle checkpoint and sexual differentiation.

Reports on the roles of p38 and c-Jun NH[2]-terminal protein kinase (JNK) in the development of apotosis during simulated ischemia and reperfusion (SI-R) in neonatal cardiomyocytes. Reduction of cell viability; Evidence of stimulated apoptosis; Importance of reperfusion to complete the apoptotic pathway.