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[The protective effects of insulin on cardiocyte apoptosis challenged by burn serum]
Gen-Fa Lü1, Hong-Wei Shi, Guang-yuan Wang
1Department of Burns and Plastic Surgery, the 534th Hospital of PLA, Luoyang 471003, Henan, China. genfalu@yahoo.com.cn
Objective:
To investigate the protective effects of insulin on burn serum-challenged cardiocyte apoptosis and its mechanism.
Methods:
Burn-serum challenged cardiocytes were pretreated with insulin and inhibitors to pathway SB203580 and LY294002. The expression of cardiac myofilament proteins cleaved-caspase-3, Bax and phosphorylation nuclear factor-ΚB inhibitive factor α (p-IΚBα) were examined by Western blotting. The mRNA expression of tumor necrosis factor-α (TNF-α) was determined by real-time reverse transcription-polymerase chain reaction (RT-PCR). Apoptosis of cardiocyte was observed after Hoechst 33258 staining. Further blocking experiments were used to investigate the cytoprotective pathway of insulin.
Results:
Insulin could significantly decrease the expression of cleaved-caspase-3 (2.22 ± 0.30 vs. 4.84 ± 0.74, P < 0.01), Bax (1.33 ± 0.35 vs. 3.74 ± 0.65, P < 0.01), p-IΚBα (1.43 ± 0.62 vs. 3.62 ± 0.74, P < 0.01), TNF-α (0.72 ± 0.27 vs. 2.02 ± 0.63, P < 0.01) and the cardiocyte apoptosis rate [(9.4 ± 3.4)% vs. (19.1 ± 5.6)%, P < 0.01] in cardiocytes challenged by burn serum. Further blocking experiments showed that LY294002, phosphatidylinositol-3-kinase (PI3K)/Akt activation inhibitor, could mitigate the protective effects of insulin. Meanwhile, SB203580, an inhibitor of p38 mitogen-activated protein kinase (p38MAPK) pathway, was able to inhibit cardiocyte injury challenged by burn serum, and it was as effective as insulin.
Conclusion:
For cardiocytes challenged by burn serum, insulin may decrease inflammatory cytokine expression and apoptosis via regulating PI3K/Akt and p38MAPK pathway.
Insights
Insulin protects heart cells from burn serum injury by reducing apoptosis and inflammation. It works by activating the PI3K/Akt and p38MAPK pathways, offering a potential therapeutic target.
Area of Science:
- Cardiology
- Molecular Biology
- Biochemistry
Background:
- Burn serum can induce apoptosis in cardiocytes.
- Understanding the protective mechanisms against burn serum-induced cardiac injury is crucial.
Purpose of the Study:
- To investigate the protective effects of insulin on burn serum-challenged cardiocyte apoptosis.
- To elucidate the underlying molecular mechanisms involving PI3K/Akt and p38MAPK pathways.
Main Methods:
- Cardiocytes were challenged with burn serum and pretreated with insulin, SB203580 (p38MAPK inhibitor), and LY294002 (PI3K/Akt inhibitor).
- Protein expression (cleaved-caspase-3, Bax, p-IκBα) and mRNA expression (TNF-α) were analyzed using Western blotting and RT-PCR.
- Cardiocyte apoptosis was assessed via Hoechst 33258 staining.
Main Results:
- Insulin significantly reduced cleaved-caspase-3, Bax, p-IκBα, TNF-α expression, and cardiocyte apoptosis rate.
- Inhibiting the PI3K/Akt pathway with LY294002 diminished insulin's protective effects.
- SB203580 inhibited burn serum-induced cardiocyte injury, demonstrating efficacy comparable to insulin.
Conclusions:
- Insulin exerts protective effects against burn serum-induced cardiocyte apoptosis.
- These effects are mediated through the regulation of the PI3K/Akt and p38MAPK signaling pathways.
- Insulin may represent a therapeutic strategy for mitigating burn-related cardiac complications.
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