Objectives On the basis of hypertrophic cardiomyocytes induced by endothelin 1 (ET-1), the present study aimed at investigating whether the effects of Ginsenosides-Rbl (Gs-Rb1) inhibiting cardiomyocyte hypertrophy were mediated by protein kinase C (PKC) in vitro.
Methods Neonatal rat cardiomyocytes, in vitro, were randomly divided into control group, Gs-Rb1 group, ET-1 group, Gs-Rb1 + ET-1 group, ET-1 + CHE (chelerythrine, PKC inhibitor) group, Gs-Rb1 + ET-1 + CHE group. The concentration of ET-1, Gs-Rb1 and CHE was 10-2 uMol/L, 200 uMol/L and 10 uMol/L. After 96 hour, Cell surface area, total protein content concentration, PKC activity, c-fos and c-jun were assayed, respectively.
Results 1. The cell surface area in Gs-Rb1 + ET-1 group was significantly decreased than in ET-1 group (P = 0.000); there was no significance between Gs-Rb1 + ET-1 + CHE and Gs-Rb1 + ET-1 group (P = 0.569). 2. The total protein content in Gs-Rb1 + ET-1 group was significantly decreased than in ET-1 group (P = 0.000), there was no significance between Gs-Rb1 + ET-1 + CHE and Gs-Rb1 + ET-1 group (P = 0.753). 3. compared to ET-1 group, Gs-Rb1 + ET-1 group significantly increased PKC activity (66.2 ± 2.2%), which was stronger than in Gs-Rb1 + ET-1 + CHE group (3.45 ± 0.7-fold, p = 0.000). 4. The mRNA (2.07 ± 0.09-fold, p = 0.000) and protein (5.48 ± 0.7-fold, p = 0.000) of c-fos was significantly higher in ET-1 group than in control group. Compared to ET-1 group, Gs-Rb1 + ET-1 group (mRNA: 89.8 ± 4.1%, p = 0.000; protein: 80.8 ± 3.6%, p = 0.000) and ET-1 + CHE group significantly inhibited c-fos (mRNA: 94.1 ± 5.9%, p = 0.000; protein: 79.4 ± 1.9%, p = 0.000), which was further inhibited than in Gs-Rb1 + ET-1 + CHE group. 5. compared with control group, ET-1 group significantly increased c-jun (mRNA: 1.98 ± 0.16-fold, p = 0.000; protein: 5.44 ± 0.5-fold, p = 0.000); compared to ET-1 group, c-jun in Gs-Rb1 + ET-1 group (mRNA:72.0 ± 3.7%, p = 0.000; protein: 87.7 ± 4.1%, p = 0.000) or in ET-1 + CHE group (mRNA:68.4 ± 3.1%, p = 0.000; protein: 96.7 ± 2.7%, p = 0.000) was significantly inhibited, which was lowest than in Gs-Rb1 + ET-1 + CHE group.
Conclusions Gs-Rb1 may inhibit cardiomyocyte hypertrophy mediated by ET-1, which was adjusted by PKC system at least.
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