RESUMEN
PURPOSE: To investigate the effect of 4-phenylbutyric acid (4-PBA) on intermittent hypoxia (IH)-induced liver cell injury and to clarify the underlying mechanisms. METHODS: L02 cells (normal human liver cells) were cultured in normoxic condition or subjected to intermittent hypoxia for 4, 8, and 12 h. A part of hypoxia-treated L02 cells was applied with 4-PBA 1 h before exposure to hypoxia. The effect of 4-PBA on liver injury, hepatocyte apoptosis, endoplasmic reticulum stress (ERS), and PERK-eIFa2-ATF4-CHOP apoptotic pathway was investigated. RESULTS: (1) IH caused apoptosis in hepatocyte; (2) IH caused ERS in hepatocyte; (3) IH caused hepatic injury; (4) 4-PBA attenuated IH-induced liver cell injury; (5) 4-PBA protected liver cell from IH-induced apoptosis; (6) 4-PBA suppressed ERS-related apoptotic pathway (PERK-eIFa2-ATF4-CHOP), but did not suppress IH-induced unfold protein reaction (UPR). CONCLUSIONS: 4-PBA could protect liver cells by suppressing IH-induced apoptosis mediated by ERS, but not by reducing the UPR.
Asunto(s)
Apoptosis/efectos de los fármacos , Supervivencia Celular/efectos de los fármacos , Retículo Endoplásmico/efectos de los fármacos , Retículo Endoplásmico/fisiología , Hepatocitos/efectos de los fármacos , Hepatocitos/fisiología , Hipoxia/complicaciones , Hipoxia/fisiopatología , Fenilbutiratos/farmacología , Supervivencia Celular/fisiología , Células Cultivadas , Humanos , Respuesta de Proteína Desplegada/efectos de los fármacosRESUMEN
Pale, soft, and exudative (PSE) meat can cause consumer dissatisfaction and economic losses. This study determined meat quality, glycolytic enzyme activity, and differential gene expression in the longissimus lumborum (LL) and semimembranosus (SM) of normal and PSE pork carcasses. The SM did not result in PSE meat. Hexokinase, lactate dehydrogenase, and pyruvate kinase activities were lower in the SM of PSE carcasses than in the normal carcasses. Functional enrichment analysis revealed that immune, inflammatory, and muscle fibre genes were significantly enriched in PSE pork. More specifically, PPP1R3G and MSS51 may be key genes regulating pork quality in the SM. Meanwhile, the differential expression of PLVAB, ADIPOQ, LEP, MYH4, MYH7, MYL3, MYL6B, FOS, ATF3, and HSPA6 may induce PSE formation in the LL. These results may provide insights into PSE pork formation mechanisms and reveal candidate genes for improving meat quality after validation.