ABSTRACT
The present study investigated the association between the levels of plasma tumor necrosis factor-α (TNF-α), interleukin (IL)-6, IL-8, high-sensitivity C-reactive protein and fibrinogen levels of patients with acute respiratory distress syndrome (ARDS) with ARDS treatment outcome and duration of mechanical ventilation, with the aim of improving the efficacy of ARDS therapy. A total of 140 patients with ARDS were randomly divided into groups A and B, with 70 patients in each group. The patients in group A received a combination of conventional treatment and comprehensive treatment (test group) and the patients in group B were treated with conventional therapy only (control group). Elbow venous blood was obtained from each patient in the morning prior to treatment, on the 3rd day of treatment and on the 5th day of treatment. The levels of inflammatory factors, the clinical effects and the duration of mechanical ventilation of the two groups were statistically analyzed. The levels of IL-6, TNF-α and IL-8 in patients from group A were significantly reduced compared with those from group B (P<0.05). Additionally, the oxygenation index and arterial partial oxygen pressure of patients in group A were significantly higher compared with group B patients (P<0.05), the duration of mechanical ventilation of group A was decreased compared with that of group B (P<0.05) and the overall response rate of group A was >90%, whereas group B had a response rate of 80.0%. These results indicate that the treatment administered to patients in group A exhibited an improved clinical efficacy. The combination of comprehensive and conventional therapy may effectively reduce the levels of inflammatory factors and the inflammatory response, and these levels may be important for the effective treatment of ARDS and in reducing treatment duration. Therefore the current study may improve upon current clinical practice.
ABSTRACT
Heat shock protein 70 (HSP70) maintains Ca(2+) homeostasis in PC12 cells, which may protect against apoptosis; however, the mechanisms of neuroprotection are unclear. Therefore, in this study, we examined Ca(2+) levels in PC12 cells transfected with an exogenous lentiviral HSP70 gene expression construct, and we subsequently subjected the cells to ischemia-hypoxia/reoxygenation injury. HSP70 overexpression increased neuronal viability and ATPase activity, and it decreased cellular reactive oxygen species levels and intracellular Ca(2+) concentration after hypoxia/reoxygenation. HSP70 overexpression enhanced the protein and mRNA expression levels of sarcoplasmic/endoplasmic reticulum Ca(2+)-ATPase (SERCA), but it decreased the protein and mRNA levels of inositol 1,4,5-trisphosphate receptor (IP3R), thereby leading to decreased intracellular Ca(2+) concentration after ischemia-hypoxia/reoxygenation. These results suggest that exogenous HSP70 protects against ischemia-hypoxia/reoxygenation injury, at least in part, by maintaining cellular Ca(2+) homeostasis, by upregulating SERCA expression and by downregulating IP3R expression.
ABSTRACT
OBJECTIVE: To evaluate the effect of melittin and 5-Fu, DDP, and TXT on human gastric cancer cell line BGC-823 and to primarily explore their possible mechanisms. METHODS: Median effect analysis was employed to determine the interaction between melittin and 5-Fu, DDP, TXT by analyzing the relationship between fraction affected (FA) and the combination index (CI) acquired from the dose-effect curve. Expressions of chemotherapeutic agent-associated genes of BGC-823 cells with or without treatment were measured by real-time fluorescent quantitative PCR. RESULTS: (1) Both melittin and chemotherapeutic agents inhibited the growth of BGC-823. (2) For BGC-823 cells were acted by 5-Fu +melittin, when FA ranged between 0.35-0.75, CI was less than 1. For BGC-823 cells were acted by DDP + melittin, when FA ranged 0.55 or so, CI = 1; when Fa ranged below 0.55, CI was less than 1. For BGC-823 cells were acted by TXT + melittin, CI less than 1 could be seen in the whole interval. (3) After treatment suppressed were the expressions of chemotherapeutic agent-associated genes of BGC-823 cells such as thymidylate synthetase (TS), excision repair cross-complementing gene 1 (ERCC1), breast cancer susceptibility gene 1 (BRCA1), beta-tubulin III (TUBB3), and microtubule-associated protein tau (MAPT). CONCLUSIONS: Melittin had a synergistic effect on the cytotoxicity of chemotherapeutic agents. The possible mechanisms might be associated with down-regulating chemotherapeutic agent-associated genes.
