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Anti-inflammatory effect of sodium butyrate preconditioning during myocardial ischemia/reperfusion.

Hu X, Zhang K, Xu C, Chen Z, Jiang H - Exp Ther Med (2014)

Bottom Line: The results demonstrated that pretreatment with sodium butyrate (300 mg/kg) significantly reduced the infarct size, as well as the levels of LDH and CK (P<0.05).In addition, sodium butyrate (300 mg/kg) was shown to significantly inhibit the I/R-induced increase in the level of MDA and reduction in the level of SOD (P<0.05).Furthermore, treatment with sodium butyrate (300 mg/kg) was found to significantly inhibit the expression of TNF-α, IL-6 and HMGB1 induced by I/R injury (P<0.05).

View Article: PubMed Central - PubMed

Affiliation: Department of Cardiology, Renmin Hospital of Wuhan University, Cardiovascular Research Institute of Wuhan University, Wuhan, Hubei 430060, P.R. China.

ABSTRACT
High mobility group box 1 protein (HMGB1) has an important role in myocardial ischemia/reperfusion (I/R) injury. Sodium butyrate, an inhibitor of histone deacetylase, has been shown to inhibit HMGB1 expression. In the present study, the effect of sodium butyrate on myocardial I/R injury in rats was investigated. Anesthetized male rats were intraperitoneally administered sodium butyrate (100 or 300 mg/kg) 30 min prior to the induction of ischemia. The rats were then subjected to ischemia for 30 min followed by reperfusion for 4 h. Infarct size, lactate dehydrogenase (LDH), creatine kinase (CK) and superoxide dismutase (SOD) activity and malondialdehyde (MDA) levels were then measured. The expression of HMGB1 was assessed using western blot analysis. The results demonstrated that pretreatment with sodium butyrate (300 mg/kg) significantly reduced the infarct size, as well as the levels of LDH and CK (P<0.05). In addition, sodium butyrate (300 mg/kg) was shown to significantly inhibit the I/R-induced increase in the level of MDA and reduction in the level of SOD (P<0.05). Furthermore, treatment with sodium butyrate (300 mg/kg) was found to significantly inhibit the expression of TNF-α, IL-6 and HMGB1 induced by I/R injury (P<0.05). In conclusion, the results from the present study suggest that preconditioning with sodium butyrate may attenuate myocardial I/R injury by inhibition of the expression of inflammatory mediators during myocardial I/R.

No MeSH data available.


Related in: MedlinePlus

Effect of sodium butyrate on HMGB1 expression during I/R (n=5 for each group). #P<0.05 vs. the SO group; ▲P<0.05 vs. the I/R group. HMGB1, high mobility group box 1 protein; SO, sham-operated control; I/R, ischemia/reperfusion; SB1, sodium butyrate (100 mg/kg); SB2, sodium butyrate (300 mg/kg).
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f5-etm-08-01-0229: Effect of sodium butyrate on HMGB1 expression during I/R (n=5 for each group). #P<0.05 vs. the SO group; ▲P<0.05 vs. the I/R group. HMGB1, high mobility group box 1 protein; SO, sham-operated control; I/R, ischemia/reperfusion; SB1, sodium butyrate (100 mg/kg); SB2, sodium butyrate (300 mg/kg).

Mentions: Following the 4-h reperfusion, HMGB1 expression was markedly increased compared with that in SO group (P<0.05). However, treatment with sodium butyrate (300 mg/kg) significantly inhibited the expression of HMGB1 (P<0.05). By contrast, treatment with a lower dose of sodium butyrate (100 mg/kg) did not provide an inhibitory effect (P>0.05; Fig. 5).


Anti-inflammatory effect of sodium butyrate preconditioning during myocardial ischemia/reperfusion.

Hu X, Zhang K, Xu C, Chen Z, Jiang H - Exp Ther Med (2014)

Effect of sodium butyrate on HMGB1 expression during I/R (n=5 for each group). #P<0.05 vs. the SO group; ▲P<0.05 vs. the I/R group. HMGB1, high mobility group box 1 protein; SO, sham-operated control; I/R, ischemia/reperfusion; SB1, sodium butyrate (100 mg/kg); SB2, sodium butyrate (300 mg/kg).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4061237&req=5

f5-etm-08-01-0229: Effect of sodium butyrate on HMGB1 expression during I/R (n=5 for each group). #P<0.05 vs. the SO group; ▲P<0.05 vs. the I/R group. HMGB1, high mobility group box 1 protein; SO, sham-operated control; I/R, ischemia/reperfusion; SB1, sodium butyrate (100 mg/kg); SB2, sodium butyrate (300 mg/kg).
Mentions: Following the 4-h reperfusion, HMGB1 expression was markedly increased compared with that in SO group (P<0.05). However, treatment with sodium butyrate (300 mg/kg) significantly inhibited the expression of HMGB1 (P<0.05). By contrast, treatment with a lower dose of sodium butyrate (100 mg/kg) did not provide an inhibitory effect (P>0.05; Fig. 5).

Bottom Line: The results demonstrated that pretreatment with sodium butyrate (300 mg/kg) significantly reduced the infarct size, as well as the levels of LDH and CK (P<0.05).In addition, sodium butyrate (300 mg/kg) was shown to significantly inhibit the I/R-induced increase in the level of MDA and reduction in the level of SOD (P<0.05).Furthermore, treatment with sodium butyrate (300 mg/kg) was found to significantly inhibit the expression of TNF-α, IL-6 and HMGB1 induced by I/R injury (P<0.05).

View Article: PubMed Central - PubMed

Affiliation: Department of Cardiology, Renmin Hospital of Wuhan University, Cardiovascular Research Institute of Wuhan University, Wuhan, Hubei 430060, P.R. China.

ABSTRACT
High mobility group box 1 protein (HMGB1) has an important role in myocardial ischemia/reperfusion (I/R) injury. Sodium butyrate, an inhibitor of histone deacetylase, has been shown to inhibit HMGB1 expression. In the present study, the effect of sodium butyrate on myocardial I/R injury in rats was investigated. Anesthetized male rats were intraperitoneally administered sodium butyrate (100 or 300 mg/kg) 30 min prior to the induction of ischemia. The rats were then subjected to ischemia for 30 min followed by reperfusion for 4 h. Infarct size, lactate dehydrogenase (LDH), creatine kinase (CK) and superoxide dismutase (SOD) activity and malondialdehyde (MDA) levels were then measured. The expression of HMGB1 was assessed using western blot analysis. The results demonstrated that pretreatment with sodium butyrate (300 mg/kg) significantly reduced the infarct size, as well as the levels of LDH and CK (P<0.05). In addition, sodium butyrate (300 mg/kg) was shown to significantly inhibit the I/R-induced increase in the level of MDA and reduction in the level of SOD (P<0.05). Furthermore, treatment with sodium butyrate (300 mg/kg) was found to significantly inhibit the expression of TNF-α, IL-6 and HMGB1 induced by I/R injury (P<0.05). In conclusion, the results from the present study suggest that preconditioning with sodium butyrate may attenuate myocardial I/R injury by inhibition of the expression of inflammatory mediators during myocardial I/R.

No MeSH data available.


Related in: MedlinePlus