Calcineurin contributed to tumor necrosis factor alpha-induced cardiomyocyte hypertrophy in rats / 中国应用生理学杂志

<p><b>OBJECTIVE</b>To investigate whether calcineurin (CaN) contribute to tumor necrosis factor alpha (TNF-alpha)-induced cardiomyocyte hypertrophy.</p><p><b>METHODS</b>The protein content was assayed with lowry's method. The cardiomyocytes volumes were measured by computer photograph analysis system. The protein synthesis was assayed with [3H]-leucine incorporation method. [Ca2+]i transient was measured by Till image system by cell-loading Fura-2/AM. The expression of CaN was determined by Western blot.</p><p><b>RESULTS</b>(1) (CsA (0.2 micromol/L), a selective CaN inhibitor, significantly suppressed the increase of protein content, [3H]-leucine incorporation and cell size induced by TNF-alpha. (2) CsA (0.2 micromol/L) significantly suppressed the elevation of the amplitude of the spontaneous Ca2+ transients induced by TNF-alpha in cultured ventricular myocytes from the neonatal rat. (3) TNF-alpha significantly increased the expression of CaN.</p><p><b>CONCLUSION</b>Ca(2+) -CaN signaling pathway are involved in cardiomyocyte hypertrophy induced by TNF-alpha in rats.</p>

Comparing effects of U50488H, prazosin and/or propranolol on cardiac hypertrophy induced by NE in rat / 中国应用生理学杂志

<p><b>OBJECTIVE</b>To demonstrate the inhibitory effect of kappa-opioid receptor activation by U50488H on hypertrophy induced by NE in cultured neonatal rat cardiac myocytes and compare its effect with that of prazosin and propranolol.</p><p><b>METHODS</b>The cellular proliferation was determined with crystal violet staining. The protein content was assayed with Lowry's method. The cardiomyocytes volumes were measured by computer photograph analysis system. The protein synthesis was assayed with [3H]-lencine incorporation method.</p><p><b>RESULTS</b>(1) NE significantly induced the increase of protein content, [3H]-leucine incorporation and cell size without a concomitant increase in cell number in low serum medium. OThese responses were partially suppressed by prazosin or propranolol alone and completely abolished by both in combination. U50488H significantly inhibited the NE-induced increase of protein content, [3H]-leucine incorporation and cell size. The inhibitory effects of U50488H on NE-induced cardiac hypertrophy were greater than either prazosin or propranolol, but comparable to combination of both.</p><p><b>CONCLUSION</b>NE, acting via both alpha1- and beta-adrenergic pathway, stimulates myocyte hypertrophy. Stimulating kappa-opioid receptor significantly inhibits NE-induced cardiac hypertrophy, which may be related with alpha1- and beta1-adrenergic pathway.</p>

Ca2+ is involved in tumor necrosis factor-alpha induced cardiomyocyte hypertrophy through PI3-kinase pathway in rats / 中国应用生理学杂志

<p><b>OBJECTIVE</b>To investigate whether Ca2+ contribute to cardiomyocyte hypertrophy induced by tumor necrosis factor-alpha (TNF-alpha) through PI3-kinase pathway.</p><p><b>METHODS</b>The protein content was assayed with Lowry's method. The cardiomyocytes volumes were measured by computer photograph analysis system. The protein synthesis was assayed with [3H]-leucine incorporation method. [Ca2+]i transient was measured by Till image system by cell-loading Fura-2/AM.</p><p><b>RESULTS</b>(1) TNF-alpha significantly induced the increase of protein content, [3H]-leucine incorporation and cell size. These responses were significantly suppressed by LY294002, a selective PI3-kinase inhibitor. Verapamil, L-type calcium channels antagonist, slightly attenuated TNF-alpha-induced these responses. (2) TNF-alpha increased the amplitude of the spontaneous Ca2+ transients in cultured ventricular myocytes from the neonatal rat; PI3-kinase inhibitor LY294002 could suppress the elevation induced by TNF-alpha, but calcium antagonist verapamil took the minor effects of TNF-alpha on [Ca2+]i metabolism.</p><p><b>CONCLUSION</b>Increasing the intercellular free Ca2+ level may play an essential role in TNF-alpha-induced cardiomyocyte hypertrophy through PI3-kinase pathway in rats, while L-type calcium channel takes the minor effects on it.</p>