RESUMO
Objective@#To investigate the effects of sulforaphane on lipopolysaccharide (LPS)- induced cardiac myocytes hypertrophy of rats and study its possible mechanism.@*Methods@#The hypertrophic primary cardiac cells of neuonatal rats were divided into control group, LPS-induced group, JAK2 inhibitor group, low-, middle-, and high-dose sulforaphane groups. The cells in all groups, except for control group, were intervened by LPS (1 mg/L). The low-, middle-, and high-dose sulforaphane groups were treated with 10, 20, 40 μg/ml sulforaphane respectively. The JAK2 inhibitor group was treated with 10 nmol/L of JAK2 inhibitor for 24 h. Computer photograph analysis system was used to determine the cardiomyocyte volume, BCA kit was used to analyze the total protein concentration, ELISA kit was used to observe the expression levels of inflammatory cytokine (including IL-6 and TNF-α), and the Western Blot technology was used to analyze the expression levels of the related proteins in JAK2/STAT3 signaling pathway.@*Results@#Compared with control group, the cell volume (1 635.71 ± 154.84 μm3, 1 450.06 ± 140.13 μm3, 1 194.51 ± 134.76 μm3 vs. 1 854.28 ± 181.37 μm3) and the levels of protein (20.14 ± 2.11 μg, 17.59 ± 1.64 μg, 14.27 ± 1.47 μg vs. 23.17 ± 2.56 μg) in low-, medium-, high- dose of sulforaphane groups were significantly decreased (P<0.05). The levels of IL-6 (1 410.08 ± 255.17 pg/ml, 1 065.61 ± 210.37 pg/ml, 790.09 ± 140.28 pg/ml vs. 1 804.07 ± 275.34 pg/ml) and TNF-α (164.16 ± 27.51 pg/ml, 130.13± 22.08 pg/ml, 92.27 ±12.16 pg/ml vs. 182.42 ± 30.37 pg/ml) in low-, medium-, high- dose of sulforaphane groups were significantly decreased (P<0.05). The expression levels of p-JAK2/JAK2 (0.39 ± 0.05, 0.27 ± 0.04, 0.21 ± 0.03 vs. 0.54 ± 0.07) and p-STAT3 (0.47 ± 0.05, 0.25 ± 0.03, 0.18 ± 0.03 vs. 0.53 ± 0.06) in low-, medium-, high- dose of sulforaphane groups were also significantly decreased (P<0.05).@*Conclusions@#Sulforaphane has a protective effect on LPS-induced cardiac hypertrophy, which is partially via inhibiting inflammatory response via suppressing the activation of JAK2/STAT3 signaling pathway.