September 29, 2007AJP Heart and Circulatory PhysiologyOpen Access

p38 and ERK1/2 MAPKs mediate the interplay of TNF-α and IL-10 in regulating oxidative stress and cardiac myocyte apoptosis

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Population

Isolated adult cardiac myocytes from Sprague-Dawley male rats

Comparison

Exposure to TNF-alpha, IL-10, and IL-10 +… vs Untreated cells or individual treatments…

Design

Preclinical

Follow-up

4 hours

Authors

SDSanjiv DhingraSt. Boniface Hospital ASAnita SharmaNepean Hospital DSDinender K. SinglaUniversity of Central Florida

Discussion

Member takes

Implication

IL-10/ERK protection in myocytes is hypothesis-generating; leaves open translation to human inflammatory cardiomyopathy.

Structured PICO

Population

Isolated adult cardiac myocytes from Sprague-Dawley male rats

Intervention

Exposure to TNF-alpha (10 ng/ml), IL-10 (10 ng/ml), and IL-10 + TNF-alpha (ratio 1) for 4 h, with or without p38 MAPK inhibitor (SB-203580) or ERK pathway inhibitor (PD-98059)

Comparator

Untreated cells or individual treatments compared to combinations

Outcome

Oxidative stress (ROS production) and cardiac myocyte apoptosis (cell injury, number of apoptotic cells, Bax-to-Bcl-xl ratio)surrogate

This preclinical study demonstrates that p38 and ERK1/2 MAPKs are essential in mediating the interactive effects of TNF-alpha and IL-10 on oxidative stress and apoptosis in cardiac myocytes.

Cite This Study

Dhingra et al. (2007) studied this question.

synapsesocial.com/papers/6a6f85aff44fa9f079dcfa03 https://doi.org/10.1152/ajpheart.00919.2007

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p38 and ERK1/2 MAPKs mediate the interplay of TNF-α and IL-10 in regulating oxidative stress and cardiac myocyte apoptosis

Discussion

Member takes

Implication

Structured PICO

Cite This Study

p38 and ERK1/2 MAPKs mediate the interplay of TNF-α and IL-10 in regulating oxidative stress and cardiac myocyte apoptosis

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Also Consider

Also Consider