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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: OBJECTIVE, METHODS, RESULTS. Meshes: Animals, Apoptosis, Apoptosis Inducing Factor, Atrial Natriuretic Factor, Benzophenanthridines, Biomarkers, DNA Fragmentation, Disease Models, Animal, In Situ Nick-End Labeling, In Vitro Techniques, Male, Models, Biological, Myocardial Contraction, Myocardial Infarction, Myocardium, Phosphorylation, Protein Kinase C-delta, Proto-Oncogene Proteins c-akt, Rats, Rats, Wistar, Signal Transduction, Time Factors, bcl-Associated Death Protein.
user
Does chelerythrine treatment influence the balance of pro- and anti-apoptotic signaling pathways in the remote myocardium after infarction? Context: Apoptotic processes may be implicated in the molecular pathomechanisms of ventricular remodeling after myocardial infarction (MI). The modulation of apoptosis by pro- and anti-apoptotic pathways in the myocardium remote from the infarction, including its link to protein kinase C (PKC), was focus of the present study. Rats were subjected to MI by LAD ligation in situ. Some animals were pretreated with the PKC inhibitor chelerythrine. After 1 h up to 28 days, pro- and anti-apoptotic signals (caspase-3, Bcl-2/Bax ratio, Akt, Bad), and marker of apoptosis execution (DNA laddering, TUNEL) were quantified in the myocardium remote from the infarction. Activation of caspase-3, a pro-apoptotic shift of the Bcl-2/Bax ratio, and DNA fragmentation were observed as early as 3 h after infarction and persisted up to 28 days. Akt- and Bad-phosphorylation was unchanged. Chelerythrine markedly reduced DNA fragmentation. Caspase-3 activation was unchanged. Surprisingly, Bad and Akt phosphorylation were highly increased (180% and 750% of control).
assistant
Chelerythrine influences the balance of pro- and anti-apoptotic pathways in the remote myocardium after infarction, with an inhibition of proapoptotic and an activation of anti-apoptotic signals. Final Decision: yes