RESUMEN
Lipid storage droplet protein 5 (LSDP5) is specifically expressed in tissues with high oxidative metabolism such as liver and heart. The present study aimed to explored the role of LSDP5 in sodium palmitateinduced lipotoxicity in LO2 normal human liver cells. LO2 cells were treated with various concentrations of sodium palmitate (25, 50, 75, 100, 125 and 150 µmol/l) for 12, 24 and 48 h, and cell viability was determined by Cell Counting Kit8. Subsequently, LO2 cells were exposed to 100 µmol/l sodium palmitate for 48 h to induce lipotoxicity (Model). Lipotoxicity Model LO2 cells were also transfected with pCMV5LSDP5 overexpression vector, and reactive oxygen species (ROS) production, mitochondrial membrane potential (MMP) and apoptotic rates were measured. The contents of nonesterified fatty acid (NEFA), malondialdehyde (MDA) and superoxide dismutase (SOD) were also measured. The expression levels of LSDP5, and apoptosis, mitochondrial, lipid metabolismrelated factors were detected using reverse transcriptionquantitative polymerase chain reaction and western blot assays. The results indicated that sodium palmitate exposure inhibited cell viability and induced lipotoxicity in LO2 cells. LSDP5 overexpression decreased ROS and apoptotic rates, and reduced NEFA and MDA content. LSDP5 transfection rescued the loss of MMP and elevated SOD content in lipotoxicity Model LO2 cells. In addition, LSDP5 upregulated the expression levels of Bcell lymphoma2, acetylCoA carboxylase1/2 and fatty acid synthase (Fas), whereas the expression levels of activatedcaspase3, Bcl2associated X protein, cytochrome c, cytochrome c oxidase subunits IV, carnitine palmitoyltransferase 1a and peroxisome proliferatoractivated receptors α levels were downregulated. LSDP5 may produce a protective effect on sodium palmitateinduced lipotoxicity in LO2 cells by regulating lipid metabolismrelated factors.
Asunto(s)
Regulación de la Expresión Génica/efectos de los fármacos , Hepatocitos/efectos de los fármacos , Metabolismo de los Lípidos/efectos de los fármacos , Ácido Palmítico/farmacología , Perilipina-5/genética , Acetil-CoA Carboxilasa/genética , Acetil-CoA Carboxilasa/metabolismo , Apoptosis/efectos de los fármacos , Apoptosis/genética , Línea Celular , Relación Dosis-Respuesta a Droga , Acido Graso Sintasa Tipo I/genética , Acido Graso Sintasa Tipo I/metabolismo , Ácidos Grasos no Esterificados/metabolismo , Hepatocitos/citología , Hepatocitos/metabolismo , Humanos , Metabolismo de los Lípidos/genética , Malondialdehído/metabolismo , Potencial de la Membrana Mitocondrial/efectos de los fármacos , Mitocondrias/efectos de los fármacos , Mitocondrias/metabolismo , Estrés Oxidativo , PPAR alfa/genética , PPAR alfa/metabolismo , Perilipina-5/metabolismo , Proteínas Proto-Oncogénicas c-bcl-2/genética , Proteínas Proto-Oncogénicas c-bcl-2/metabolismo , Especies Reactivas de Oxígeno/metabolismo , Transducción de Señal , Superóxido Dismutasa/genética , Superóxido Dismutasa/metabolismo , Proteína bcl-X/genética , Proteína bcl-X/metabolismoRESUMEN
Spontaneous rupture of a splenic artery aneurysm with splenic epithelioid hemangioendothelioma is a rare condition. Splenic artery aneurysm can be complicated by rupture resulting in hypovolemic shock, which can be fatal if not treat properly. We report a case of a 50-year-old man who presented with sudden onset of left upper quadrant pain and shock. This patient underwent splenectomy with distal pancreatectomy. His pathological diagnosis showed splenic epithelioid hemangioendothelioma.
Asunto(s)
Aneurisma Roto/patología , Hemangioendotelioma Epitelioide/patología , Rotura Espontánea/patología , Arteria Esplénica/patología , Aneurisma Roto/complicaciones , Aneurisma Roto/cirugía , Hemangioendotelioma Epitelioide/complicaciones , Hemangioendotelioma Epitelioide/cirugía , Humanos , Masculino , Persona de Mediana Edad , Pancreatectomía , Pronóstico , Rotura Espontánea/complicaciones , Rotura Espontánea/cirugía , Esplenectomía , Arteria Esplénica/cirugíaRESUMEN
Migration of metal clips into the duodenum after laparoscopic cholecystectomy is rare. We herein present two cases of migration of metal clips into the duodenum in patients who developed upper quadrant discomfort and a poor appetite after laparoscopic cholecystectomy. Gastroscopy revealed metal clips in the duodenum. In one patient, the clip dropped from the duodenum after 2 months; the other patient went to another institution to undergo duodenotomy. The mechanism underlying migration of a metal clip into the duodenum remains unclear but might be related to chronic inflammation and duodenal peristalsis. In conclusion, clinicians must remember that metal clips can migrate after laparoscopic cholecystectomy and later cause complications.
