Objective To investigate the effect of propofol on autophagy in SD rat heart during myocar-dial ischemia-reperfusion (I/R) injury. Methods Twenty-one male SD rats were randomly divided into three groups as follows (n = 7): the sham operation group, in which rats underwent sham operation without tightening of the coronary artery sutures; the myocardial ischemia-reperfusion group , in which rats were induced by occlud-ing the left anterior descending coronary artery for 30 min , followed by 120 min reperfusion and 0.9% NaCl in-fusion at 3 mL/(kg·h) at 10 min before occluding the left anterior descending coronary artery; the myocardial ischemia- reperfusion- propofol group, in which rats underwent I/R and propofol infusion at 6 mg/(kg·h) at 10 min before occluding the left anterior descending coronary artery. Before tightening of the coronary artery, at 30 min post-tightening of the coronary artery and at 120 min post-reperfusion, HR、 LVSP and ± dp/dtmax of rats were recordedin each group. Atter 120 min post-reperfusion, the serum concentrations of cTnT was measured. The in-jured cardiac tissue was collected to investigate the ultrastructure change under the TEM and to determine the levels of mTOR and p-mTOR. Results No signifcant differences in HR, LVSP and ± dp/dtmax before tighten-ing of the coronary artery. But, at 30 min post- tightening of the coronary artery, compared with groupⅠ, the HR, LVSP and ±dp/dtmax were significantly decresed in groupⅡ and Ⅲ(P < 0.05). Then, at 2 h post-reper-fusion, compared with groupⅠ, the HR, LVSP, ±dp/dtmax and the level of p-mTOR were significantly de-creased, but the serum concentration of cTnT was significantly increased in groupⅡ(P < 0.05); but, compared with groupⅡ, the HR, LVSP, ± dp/dtmax and the level of p-mTOR were significantly increased, the serum concentration of cTnT and the level of mTOR were significantly decreased in group Ⅲ(P < 0.05). Conclusions These data suggest that propofol could heighten the level of p-mTOR, and attenuate the expression of mTOR dur-ing the myocardial ischemia-reperfusion injury in SD rats.

OBJECTIVE: To investigate the effects of combined inhibition of signal transducer and activator of transcription 3 (STAT3) and hypoxia-inducible factor-1α (HIF-1α) in the enhancement of chemosensitivity of the model of human laryngeal squamous cacinoma in nude mice. METHOD: Model nude mice were divided into six groups randomly: control group(A) , cisplatin group(B) , cisplatin and AG490 group(C) , cisplatin and HIF-1α⁻/⁻ group (D), cisplatin combined AG490 and HIF-1α⁻/⁻ group (E), HIF-1α⁻/⁻ group (F) (only in calculating tumor inhibition rate). 3mg/kg cisplatin was administered by peritoneal injection for 3 days. Then cisplatin and 10 mg/kg AG490 were administered every other day for 12 days. The expression of Ki67 and HIF-1α was detected by immunocytochemical method. Western blot was used to detect the expression of p-STAT3. RESULT: The expression of HIF-1α in group C and group D were lower than that in group B, and there were significant difference respectively (t₁ = 2.782, t₂ = 3.873, P < 0.05); The expression of HIF-1α in group E was lower than that in group C and group D respectively, and there were significant difference respectively (t₁ = 6.140, t₂ = 3.667, P < 0.01). The expression level of p-STAT3 in group C was markedly lower compared with that in group B, and there were significant difference between them (t = 17.840, P < 0.01); There were no difference between the expression level of p-STAT3 in group D and that in group B (t = 0.038, P > 0.05); The expression level of p-STAT3 in group E was significantly lower compared with that in group C and group D respectively (P < 0.01). Tumor inhibition rate of group E was higher than that in group B, group C , as well as group D respectively and there were significant difference respectively (t₁ = 5.509, P < 0.01; t₂ = 3.422, P < 0.05; t₃ = 2.718, P < 0.05 ). Ki67 index of group E was lower than that in group B, group C as well as group D respectively and there were significant difference respectively(t₁ = 8.307, P < 0.01; t₂ = 3.736, P < 0.05; t₃ = 4.524, P < 0.01). CONCLUSION Combined inhibition of STAT3 and HIF-1α could enhance chemo-sensitivity in the model of human laryngeal squamous cacinoma in nude mice.
Animals ; Antineoplastic Agents ; pharmacology ; Carcinoma, Squamous Cell ; drug therapy ; metabolism ; Cisplatin ; pharmacology ; Drug Resistance, Neoplasm ; Hypoxia-Inducible Factor 1, alpha Subunit ; genetics ; metabolism ; Ki-67 Antigen ; metabolism ; Laryngeal Neoplasms ; drug therapy ; metabolism ; Mice ; Mice, Nude ; Neoplasms, Experimental ; drug therapy ; metabolism ; STAT3 Transcription Factor ; genetics ; metabolism ; Tyrphostins ; pharmacology

Idiopathic Pulmonary Fibrosis is a chronic interstitial lung disease of unknown etiology with a short survival period, poor prognosis, and difficult to completely cure. At present, the main diagnostic method of IPF is High Resolution CT (HRCT), which has the disadvantage of high subjective impact and low repeatability. Therefore, it is necessary to develop novel biomarkers to aid in the diagnosis and prognosis of IPF. In recent years, more and more studies have focused on exosomes, whose specific regulatory mechanisms for IPF have not been fully elucidated, although it has been extensively studied in the field of malignant tamors and cardiovascular disease. In addition, exosomes can be secreted by different cells and body fluids, having potential applications in suggesting IPF risk and diagnostic prognosis.