Effect of propofol on myocardial ischemia/reperfusion injury in rats through JAK/STAT signaling pathway.

OBJECTIVE: The aim of this study was to investigate the influences of propofol on myocardial ischemia/reperfusion injury in rats through the Janus kinase/signal transducers and the activators of transcription (JAK/STAT) signaling pathway. MATERIALS AND METHODS: A total of 48 Sprague-Dawley (SD) rats were randomly divided into four groups, including: the sham-operation group (n=12), the model group (n=12), the propofol group (n=12) and the inhibitor group (n=12). The rats in the sham-operation group only received thoracotomy, without the modeling of the ischemia/reperfusion injury. The model of myocardial ischemia/reperfusion injury was established in the rats of the model group, and the rats were given normal saline for intervention. The rats in the propofol group were utilized to prepare the model of myocardial ischemia/reperfusion injury and were intervened with propofol. Meanwhile, the rats in the inhibitor group received intervention with AG490 after the establishment of myocardial ischemia/reperfusion injury model. Immunohistochemistry was applied to detect the expressions of B-cell lymphoma-2 (Bcl-2) and Bcl-2-associated X protein (Bax). Western blotting was utilized to measure the relative protein expressions of phosphorylated JAK2 (p-JAK2) and p-STAT3. The messenger ribonucleic acid (mRNA) expressions of Bax and Bcl-2 were determined via quantitative Polymerase Chain Reaction (qPCR). Furthermore, cell apoptosis was examined using terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay. RESULTS: Immunohistochemistry results showed that compared with the sham-operation group, the positive expression of Bax remarkably increased (p<0.05), while Bcl-2 notably decreased (p<0.05) in the model group, propofol group, and inhibitor group. The propofol group and inhibitor group showed a significant lower positive expression of Bax (p<0.05) and evident higher positive expression of Bcl-2 (p<0.05) when compared with the model group. However, there were no significant differences in the positive expressions of Bax and Bcl-2 between the propofol group and inhibitor group (p>0.05). According to the results of Western blotting, the relative protein expression levels of p-JAK2 and p-STAT3 proteins were remarkably elevated in the model group, propofol group and inhibitor group in comparison with those in the sham-operation group (p<0.05). Propofol group and inhibitor group exhibited remarkably lower protein expression levels of p-JAK2 and p-STAT3 compared with the model group (p<0.05). However, no significant differences were observed in the protein expressions of p-JAK2 and p-STAT3 between propofol group and inhibitor group (p>0.05). The results of qPCR manifested that the mRNA expression of Bax was notably higher (p<0.05), whereas Bcl-2 was significantly lower (p<0.05) in the model group, propofol group and inhibitor group than those of the sham-operation group. Compared with the model group, the mRNA expression of Bax was evidently declined (p<0.05), while Bcl-2 was significantly elevated (p<0.05) in the propofol group and inhibitor group. Meanwhile, there were no evident differences in the mRNA expressions of Bax and Bcl-2 between the propofol group and inhibitor group (p>0.05). Subsequent TUNEL assay indicated that the model group, propofol group, and inhibitor group showed remarkably higher apoptosis rate than the sham-operation group (p<0.05). Moreover, the apoptosis rate was remarkably reduced in the propofol group and inhibitor group in comparison with the model group (p<0.05). However, no significant difference was observed in the apoptosis rate between propofol group and inhibitor group (p>0.05). CONCLUSIONS: Propofol inhibits myocardial cell apoptosis after myocardial ischemia/reperfusion injury by repressing the JAK/STAT signaling pathway.

Lung cancer patients with a previous extra-pulmonary malignancy should not be considered homogeneous: a clinicopathological analysis of 3530 surgical cases.

BACKGROUND: Lung cancer patients with a previous extra-pulmonary malignancy have been widely discussed for their postoperative prognosis. Still, whether different types of previous extra-pulmonary malignancy confer different clinicopathological features and outcomes of lung cancer patients deserves further investigation. METHODS: The medical records of patients undergoing operation for pulmonary malignancy were retrospectively reviewed. After identifying primary lung cancer out of pulmonary metastasis in patients with a history of previous extra-pulmonary malignancy, clinicopathological parameters and postoperative prognosis were compared between lung cancer patients without and with different types of previous extra-pulmonary malignancy. RESULTS: Approximately, 5.0% lung cancer patients undergoing surgery had a previous extra-pulmonary malignancy. Prior breast cancer (20%) and colorectal cancer (16%) formed the majority of these previous extra-pulmonary malignancies. Many clinicopathological features such as reason for visit, tumor size and histological subtype were significantly different between lung cancer patients without and with different types of previous extra-pulmonary malignancy (P < 0.05). Lung cancer patients with a previous occurrence of breast cancer were the most different type from patients without a previous extra-pulmonary malignancy in clinicopathological features (P < 0.05). The postoperative overall survival was not significantly different between lung cancer patients without and with different types of previous extra-pulmonary malignancy (P > 0.05). CONCLUSION: Previous extra-pulmonary malignancy was confirmed to be harmless to postoperative prognosis of lung cancer patients. Lung cancer patients with a previous extra-pulmonary malignancy, especially with a previous occurrence of breast cancer, were highly heterogeneous in clinicopathological features. These findings implied there might be a unique etiology existing in lung cancer following a previous occurrence of breast cancer.

[Clinical manifestations analysis of patients diagnosed with primary pulmonary mucosa-associated lymphoid tissue lymphoma].

Objective: To analyze the clinical features of pulmonary mucosa-associated lymphoid tissue (MALT) lymphoma. Methods: A total of 14 cases diagnosed with primary pulmonary MALT lymphoma were collected from May 2007 to May 2017 in Zhongshan Hospital, Fudan University. The clinical features, pathological characteristics, diagnosis, treatment and prognosis were retrospectively analyzed. Results: All 14 cases were pathologically diagnosed with primary pulmonary MALT lymphoma. The biopsy tissues were obtained through the Video-assisted Thoracoscopic Surgery (VATS) (4 cases), percutaneous puncture (2 cases), and bronchoscopy (8 cases). Cell types of these tumors were centrocyte-like cells (10 cases), lymphocytoid cells (2 cases), and monocytoid B cells (2 cases). The B cell clonality was detected by IgH cloning test in 4 cases and 3 of them were demonstrated with monoclonal strips. MALT1 breakup gene was positive in 3 out of 6 examined cases using fluorescence in situ hybridization (FISH). As for the treatment, 8 patients underwent chemotherapy, 5 patients underwent surgical resection and 1 patient abandoned treatment. Twelve patients were followed up to 9 years. The tumor recurrence occurred in 2 patients and resulted their death. Conclusions: The clinical manifestations of primary pulmonary MALT lymphoma are lack of specificity. The pathology, immunohistochemistry, IgH cloning test and MALT1 breakup gene tested by FISH are the criteria for diagnosis.