RESUMEN
<p><b>OBJECTIVE</b>To explore the protective effect of sodium tanshinone IIA sulfonate (STS) on small: intestine injury in rats with sepsis and its possible mechanism.</p><p><b>METHODS</b>According to a random number table, 24 Tats were randomly divided into 3 groups: sham operation group (sham group), sepsis model group (model group) and STS treatment group (STS group), with 8 Tats in each group. A rat model of sepsis was induced by cecal ligation and puncture (CLP) for 5 h. STS (1 mg/kg) was slowly injected through the right external jugular vein after CLP. The histopathologic changes in the intestine tissue were observed under a light microscope, and the intestinal epithelial cell apoptosis was evaluated by terminal deoxynucleoddyl transferase (TdT)-mediated dUTP nick-end labeling (TUNEL) method. The expressions of Bcl-2, Bax and nuclear factor κB (NF-κB) p65 in the intestinal tissue was determined by Western blot. The levels of tumor necrosis factor α (TNF-α) and interleukin 6 (IL-6) in the intestinal tissue were determined using enzyme-linked immuno-sorbent assay (ELISA).</p><p><b>RESULTS</b>Obvious injuries were observed in the intestinal tissue in the CLP group compared with the sham group. The expression of NF-κB p65 and the levels of TNF-α and IL-6 were up-regulated after CLP, the apoptosis of intestinal epithelial cells was increased after CLP, and the ratio of Bcl-2 to Bax was decreased. STS post-treatment could attenuate the injury on the intestinal tissue induced by CLP, decrease the apoptosis of intestinal treatment epithelial cells and the levels of NF-κB p65, TNF-α and IL-6, and increase the ratio of Bcl-2 to Bax.</p><p><b>CONCLUSION</b>STS can protect the small intestine in rats with sepsis, and the mechanism may be associated with the inhibition of intestinal epithelial apoptosis and the reduction of activation of inflammatory cytokines.</p>
Asunto(s)
Animales , Masculino , Ratas , Apoptosis , Interleucina-6 , Metabolismo , Intestino Delgado , Heridas y Lesiones , Metabolismo , Patología , Fenantrenos , Farmacología , Usos Terapéuticos , Sustancias Protectoras , Farmacología , Usos Terapéuticos , Ratas Wistar , Sepsis , Quimioterapia , Patología , Factor de Transcripción ReIA , Metabolismo , Factor de Necrosis Tumoral alfa , Metabolismo , Proteína X Asociada a bcl-2 , MetabolismoRESUMEN
<p><b>OBJECTIVE</b>To investigate the changes of proto-oncogene c-fos, c-jun mRNA expression in angiotensin II (Ang II)-induced hypertrophy and effects of tanshinone II A (Tan) in the primary culture of neonatal rat cardiomyocytes.</p><p><b>METHOD</b>Twelve neonatal Wistar rats aged one day old of clean grade and both sexes were selected to isolate and culture cardiomyocytes. The cardiomyocytes were divided into: normal control group, Ang II (10(-6) mol x L(-1)) group, Ang II (10(-6) mol x L(-1)) +Tan (10(-8) g x L(-1)) group, Ang II (10(-6) mol x L(-1)) + valsartan (10(-6) mol x L(-1)) group, Tan (10(-8) g x L(-1)) group, valsartan (10(-6) mol x L(-1)) group. The cardiomyocyte size was determined by phase contrast microscope, the rate of protein synthesis in cardiomyocytes was measured by 3H-leucine incorporation. The c-fos, c-jun mRNA expression of cardiomyocytes were assessed using reverse transcription polymerase chain reaction (RT-PCR).</p><p><b>RESULT</b>Ang II was added to the culture medium and 30 min later, the c-fos, c-jun mRNA expression of cardiomyocytes increased significantly (P < 0. 01). After Ang II took effect for 24 h, the rate of protein synthesis in Ang II group increased more prominently than that in normal control group (P < 0.01). After Ang II took effect for 7 days, the size of cardiomyocyte in Ang II group increased obviously (P < 0. 05). If tanshinone II or valsartan was added to the culture medium before Ang II, both of them could inhibit the increase of c-fos, c-jun mRNA expression (P < 0.01), cardiomyocyte protein synthesis rate (P < 0.01), and cardiomyocyte size (P < 0.05) induced by Ang II.</p><p><b>CONCLUSION</b>Tanshinone II could ameliorate Ang II-induced cardiomyocytes hypertrophy by inhabiting c-fos, c-jun mRNA expression.</p>
Asunto(s)
Animales , Ratas , Angiotensina II , Farmacología , Cardiomegalia , Metabolismo , Patología , Abietanos , Regulación de la Expresión Génica , Genes fos , Genética , Genes jun , Genética , Miocitos Cardíacos , Metabolismo , Patología , Fenantrenos , Farmacología , Proteínas Proto-Oncogénicas c-fos , Genética , Proteínas Proto-Oncogénicas c-jun , Genética , ARN Mensajero , Genética , Metabolismo , Ratas Wistar , Tetrazoles , Farmacología , Valina , Farmacología , ValsartánRESUMEN
<p><b>OBJECTIVE</b>To observe effects of tetrandrine (Tet) on angiotensin II (Ang II)-induced cardiomyocyte hypertrophy and the activity and expression of phosphorylated ERK1/2 (p-ERK1/2).</p><p><b>METHOD</b>In the primary culture of neonatal rat cardiomyocytes, as indexes of cardiomyocyte hypertrophy, pulsation rate was measured under phase contrast microscope. Cell size was determined by cell morphology analytical system. The total protein was determined by coomassie brilliant blue and protein synthesis rate was measured by [3H]-Leucine incorporation. ERK activity was measured by immuno-precipitation. The expression of p-ERK1/2 was assessed using Western blot.</p><p><b>RESULT</b>Tet can decrease Ang II-induced elevations of the pulsation rate, cell size, total protein and protein synthesis rate; inhibit the activity and expression of p-ERK1/2.</p><p><b>CONCLUSION</b>The anti-hypertrophic effect of Tet on Ang II-induced cardiomyocyte hypertrophy was associated with inhibition of ERK1/2 signaling pathway.</p>