Effect of Berberine on PPARα/NO Activation in High Glucose- and Insulin-Induced Cardiomyocyte Hypertrophy

Figure 3

The effect of berberine on NO concentration and NOS activity in hypertrophic cardiomyocytes induced by HGI (25.5 mmol/L glucose and 0.1 μmol/L insulin). Cardiomyocytes were pretreated with various agents for 30 min and then stimulated by HGI for 48 h. The media were then collected for measurement of NO concentration and NOS activity. Levels of NO concentration and NOS activity decreased in the HGI group, and berberine was able to reverse the decrease in NO concentration (a) and NOS activity (b) in a concentration-dependent manner. The effect of various agents, alone or in combination, on NO concentration and NOS activity is shown in (c) and (d). Fenofibrate (0.3 μmol/L), a selective PPARα agonist, or L-arginine (100 μmol/L) had effects similar to berberine (3 μmol/L). Moreover, MK886 (0.3 μmol/L), a selective PPARα antagonist, could abolish the effects of both berberine and fenofibrate. L-NAME (100 μmol/L), a NOS inhibitor, could abolish the effects of both berberine and L-arginine. Results are represented by mean ± SEM of 6 experiments. ^∗𝑃<0.05 versus control; ^#𝑃<0.05 versus HGI; ^●𝑃<0.05 versus HGI + fenofibrate (0.3 μmol/L); ^▴𝑃<0.05 versus HGI + berberine (3 μmol/L); ^▵𝑃<0.05 versus HGI + 𝐿-arginine (100 μmol/L). “+” or “−”: treatment with or without relevant reagent.

(a)

(b)

(c)

(d)