PubMed | Zunyi Medical College Zunyi, Zunyi Medical College, Affiliated Hospital of Zunyi Medical College and Virtual Medical Centre
Type: Journal Article | Journal: Oncotarget | Year: 2016
Gemcitabine and cisplatin is the first line chemotherapy for non-small cell lung cancer with high toxicity. Aidi injection is a cantharidin and astragalu-based Chinese herbs injection in China. Has Aidi injection attenuation and synergistic efficacy to GP in NSCLC? There is lack of strong evidence to prove it. To further reveal it, we systematically evaluated all related studies. We collected all studies about Aidi injection plus GP for NSCLC in Medline, Embase, Web of Science, CNKI, VIP, Wanfang Database, CBM, CCRCT, Chi-CTR, and US-clinical trials (established to June 2015). We evaluated their quality according to the Cochrane evaluation handbook of randomized controlled trials (5.1.0), extracted data following the PICO principles and synthesized the data by Meta analysis. Thirty six RCTs with 2582 NSCLC patients were included, with general methodological quality in most trials. The RR values and their 95% CI of Meta-analysis for ORR, DCR and QOL were as following: 1.28 (1.17, 1.39), 1.11(1.07, 1.15) and 1.81 (1.61, 2.03). The merged RD values and their 95% CI of Meta-analysis for myelosuppression, neutropenia, thrombocytopenia, neurotoxicity and nausea and vomiting were as following: -0.23(-0.29, -0.17), -0.17(-0.22, -0.11), -0.13(-0.18, -0.08), -0.06(-0.17, 0.05) and -0.15(-0.21, -0.10). To compare with GP alone, all differences were statistically significant. The available evidence indicates that Aidi injection plus GP can significantly increase the clinical efficacy and improve the QOL of patients with NSCLC. Aidi injection can reduce myelosuppression, neutropenia, thrombocytopenia neurotoxicity and nausea/vomiting. These indirectly reveal that Aidi injection has the attenuation and synergistic efficacy to GP chemotherapy in NSCLC.
PubMed | Zunyi Medical College Zunyi and University of Macau
Type: | Journal: Frontiers in pharmacology | Year: 2016
PubMed | Zunyi Medical College Zunyi, Xinjiang Medical University and University of Hong Kong
Type: Journal Article | Journal: American journal of translational research | Year: 2016
Sevoflurane postconditioning (SPostC) can exert myocardial protective effects similar to ischemic preconditioning. However, the exact myocardial protection mechanism by SPostC is unclear. Studies indicate that hypoxia-inducible factor-1 (HIF-1) maintains cellular respiration homeostasis by regulating mitochondrial respiratory chain enzyme activity under hypoxic conditions. This study investigated whether SPostC could regulate the expression of myocardial HIF-1 and to improve mitochondrial respiratory function, thereby relieving myocardial ischemia-reperfusion injury in rats.The myocardial ischemia-reperfusion rat model was established using the Langendorff isolated heart perfusion apparatus. Additionally, postconditioning was performed using sevoflurane alone or in combination with the HIF-1 inhibitor 2-methoxyestradiol (2ME2). The changes in hemodynamic parameters, HIF-1 protein expression levels, mitochondrial respiratory function and enzyme activity, mitochondrial reactive oxygen species (ROS) production rates, and mitochondrial ultrastructure were measured or observed.Compared to the ischemia-reperfusion (I/R) group, HIF-1 expression in the SPostC group was significantly up-regulated. Additionally, cardiac function indicators, mitochondrial state 3 respiratory rate, respiratory control ratio (RCR), cytochrome C oxidase (CThe myocardial protective function of SPostC might be associated with the improvement of mitochondrial respiratory function after up-regulation of HIF-1 expression.
PubMed | Zunyi Medical College Zunyi and Guizhou Provincial Peoples Hospital
Type: Journal Article | Journal: International journal of clinical and experimental pathology | Year: 2015
Hypercholesterolemia is an important risk factor for atherosclerosis and cholesterol treatment would cause multiple damages, including DNA damage, on endothelial cells. In this work, we have used human umbilical vein endothelial cell line (HUVEC) to explore the mechanism of cholesterol induced damage. We have found that cholesterol treatment on HUVEC could induce the expression of MCPIP1. When given 12.5 mg/L cholesterol on HUVEC, the expression of MCPIP1 starts to increase since 4 hr after treatment and at 24 hr after treatment it could reach to 10 fold of base line level. We hypothesis this induction of MCPIP1 may contribute to the damaging process and we have used siRNA of MCPIP1 in further research. This MCPIP1 siRNA (siMCPIP) could down regulate MCPIP1 by 73.4% and when using this siRNA on HUVECs, we could see the cholesterol induced DNA damage have been reduced. We have detected DNA damage by H2AX foci formation in nuclear, H2AX protein level and COMET assay. Compare to cholesterol alone group, siMCPIP group shows much less H2AX foci formation in nuclear after cholesterol treatment, less H2AX protein level in cell and also less tail moment detected in COMET assay. We have also seen that using siMCPIP1 could result in less reactive oxygen species (ROS) in cell after cholesterol treatment. We have also seen that using siMCPIP could reduce the protein level of Nox4 and p47(phox), two major regulators in ROS production. These results suggest that MCPIP1 may play an important role in cholesterol induced damage.