ABSTRACT
Sesamin, a lipid-soluble lignin originally isolated from sesame seeds, which induces cancer cell apoptosis and autophagy. In the present study, has been reported that sesamin induces apoptosis via several pathways in human lung cancer cells. However, whether mitophagy is involved in sesamin induced lung cancer cell apotosis remains unclear. This study, the anticancer activity of sesamin in lung cancer was studied by reactive oxygen species (ROS) and mitophagy. A549 cells were treated with sesamin, and cell viability, migration ability, and cell cycle were assessed using the CCK8 assay, scratch-wound test, and flow cytometry, respectively. ROS levels, mitochondrial membrane potential, and apoptosis were examined by flow cytometric detection of DCFH-DA fluorescence and by using JC-1 and TUNEL assays. The results indicated that sesamin treatment inhibited the cell viability and migration ability of A549 cells and induced G0/G1 phase arrest. Furthermore, sesamin induced an increase in ROS levels, a reduction in mitochondrial membrane potential, and apoptosis accompanied by an increase in cleaved caspase-3 and cleaved caspase-9. Additionally, sesamin triggered mitophagy and increased the expression of PINK1 and translocation of Parkin from the cytoplasm to the mitochondria. However, the antioxidant N-acetyl-L-cysteine clearly reduced the oxidative stress and mitophagy induced by sesamin. Furthermore, we found that cyclosporine A (an inhibitor of mitophagy) decreased the inhibitory effect of sesamin on A549 cell viability. Collectively, our data indicate that sesamin exerts lethal effects on lung cancer cells through the induction of ROS-mediated mitophagy and mitochondrial apoptosis.
ABSTRACT
Sesamin, a lipid-soluble lignin originally isolated from sesame seeds, which induces cancer cell apoptosis and autophagy. In the present study, has been reported that sesamin induces apoptosis via several pathways in human lung cancer cells. However, whether mitophagy is involved in sesamin induced lung cancer cell apotosis remains unclear. This study, the anticancer activity of sesamin in lung cancer was studied by reactive oxygen species (ROS) and mitophagy. A549 cells were treated with sesamin, and cell viability, migration ability, and cell cycle were assessed using the CCK8 assay, scratch-wound test, and flow cytometry, respectively. ROS levels, mitochondrial membrane potential, and apoptosis were examined by flow cytometric detection of DCFH-DA fluorescence and by using JC-1 and TUNEL assays. The results indicated that sesamin treatment inhibited the cell viability and migration ability of A549 cells and induced G0/G1 phase arrest. Furthermore, sesamin induced an increase in ROS levels, a reduction in mitochondrial membrane potential, and apoptosis accompanied by an increase in cleaved caspase-3 and cleaved caspase-9. Additionally, sesamin triggered mitophagy and increased the expression of PINK1 and translocation of Parkin from the cytoplasm to the mitochondria. However, the antioxidant N-acetyl-L-cysteine clearly reduced the oxidative stress and mitophagy induced by sesamin. Furthermore, we found that cyclosporine A (an inhibitor of mitophagy) decreased the inhibitory effect of sesamin on A549 cell viability. Collectively, our data indicate that sesamin exerts lethal effects on lung cancer cells through the induction of ROS-mediated mitophagy and mitochondrial apoptosis.
ABSTRACT
Objective To detect the contrast of vido‐assisted thoracic surgery (VATS) and conventional thoracotomy lobectomy for esophageal carcinoma .Methods 30 cases advanced esophageal carcinoma were selected in our hospital and divided into VATS group and thoracotomy group ,recorded pathological diagnosis ,operation and postoperative hospital stay and complications .Results VATS group had less bleeding ,shorter postoperative hospital stay ,less complications ,there was significant differences compared with thoracotomy group .Conclusion VATS in the treatment of advanced esophageal carcinoma have high safety ,definite curative effect ,and is worthy of extensive research and extension.
ABSTRACT
BACKGROUND: Pacing-induced atrial electrical remodeling (AER) is characterized by shortening of atrial effective refractory period (A-ERP) and its altered rate adaptation. In paroxysmal atrial fibrillation (AF), periods of AF occur with interveneing normal sinus rhythm (NSR) when atria recover from the preceding AER. Previous episodes of AF may precondition the atrial myocardium and cause different time course of AER in subsequent episodes of AF. But the influence of the preceding AER on the subsequent AER has not been described. METHODS: Four mongrel dogs were anesthetized with enflurane. After thoracotomy, silicon band with 3 pairs of electrodes was sutured to the lateral wall of the left atrium. Atrial pacing was performed after 2 wks of recovery and autonomic blockade. Pacing protocol consisted of rapid atrial pacing (RAP) at 500 bpm (for 60 min) and recovery in NSR (for 60 min) which was repeated three times. A-ERP was measured every 10 min. The same pacing protocol was repeated after pretreatment with verapamil (0.1 mg/kg/hr). RESULTS: 1) With 60 min of RAP, A-ERP decreased significantly (126+/-6 ms vs. 105+/-7 ms, p<0.005). 2) After cessation of pacing, A-ERP returned to 98% of baseline value in 15 minutes. Recovery from AER occurred faster than AER (78 vs 21 ms/h). 3) After pretreatment with verapamil, RAP decreased A-ERP from 127+/-5 ms to 116+/-5 ms. AER, the reduction in A-ERP, was significantly attenuated by pretreatment with verapamil (deltaERp=17+/-7 vs. 9+/-0.2 %, p<0.05). 4) When RAPs were repeated, AER showed a tendency of acceleration, but it was not statistically significant (deltaERp=22 ms, 24 ms, 28 ms at the end of 60 min pacing for the 1st, 2nd, 3rd pacing). CONCLUSION: RAP induced AER in conscious dog atria and it was reduced by pretreatment with calcium channel blocking agent, verapamil. Upon repeated atrial stimulations, AER did not accelerate or decelerate when the atria recovered from the preceding AER.