Biomedicine & pharmacotherapy = Biomédecine & pharmacothérapie
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Biomed. Pharmacother. · Oct 2018
Sevoflurane reduced functional connectivity of excitatory neurons in prefrontal cortex during working memory performance of aged rats.
Sevoflurane has been found to increase apoptosis and pathologic markers associated with Alzheimer disease, provoking concern over their potential contribution to postoperative cognitive dysfunction. This study aimed to evaluate the effects of sevoflurane on working memory of rats and to characterize functional connectivity between excitatory neurons in the prefrontal cortex (PFC) during working memory performance. ⋯ Sevoflurane-induced working memory impairment may depend on advanced age and anesthetic concentration. These findings also suggest, in rats, that sevoflurane-induced working memory impairment may be related to the decreased functional connectivity between PFC excitatory neurons.
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Biomed. Pharmacother. · Oct 2018
The protective effects of a novel synthetic β-elemene derivative on human umbilical vein endothelial cells against oxidative stress-induced injury: Involvement of antioxidation and PI3k/Akt/eNOS/NO signaling pathways.
Antioxidant therapy is considered as promising strategy for treating oxidative stress-induced cardiovascular disease. Bis (β-elemene-13-yl) glutarate (BEG) is a novel β-elemene derivative. Herein, we examined the antioxidant activity of BEG on human umbilical vein endothelial cells (HUVECs) after injury with hydrogen peroxide (H2O2) and investigated the mechanism involved. ⋯ BEG effects were inhibited by a PI3K inhibitor (wortmannin) and eNOS inhibitor (L-NAME). In conclusion, the present study demonstrated that BEG has antioxidant activity. Furthermore, BEG reduced H2O2-induced endothelial cells injury by the involvement of antioxidation and PI3K/Akt/eNOS/NO signaling pathways.
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Biomed. Pharmacother. · Oct 2018
Long noncoding RNA HOXD-AS1 promotes non-small cell lung cancer migration and invasion through regulating miR-133b/MMP9 axis.
HOXD antisense growth associated long noncoding RNA (HOXD-AS1) was reported to be dysregulated and exert crucial roles in tumorigenesis and progression of multiple malignancies. However, the role and mechanism of action of HOXD-AS1 in the carcinogenesis and progression of non-small lung cell cancers (NSCLC) remains largely unknown. HOXD-AS1, miR-133a and Matrix metallopeptidase 9 (MMP-9) mRNA expression were detected by quantitative real-time polymerase chain reaction assays in NSCLC tissues and cell lines. ⋯ Additionally, we found that miR-133b was a direct downstream target of HOXD-AS1 in NSCLC. miR-133b inhibition reverse the inhibitory effect of HOXD-AS1 knockdown on the proliferation, migration, and invasion of NSCLC cells. Furthermore, HOXD-AS1 positively regulated the expression of MMP-9 (a target of miR-133b) in NSCLC cells. These results suggest that HOXD-AS1 might be a potential prognostic biomarker and a novel therapeutic target for treating NSCLC.
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Biomed. Pharmacother. · Oct 2018
Controlled Clinical TrialCharacterization of cardiovascular depression effect for propofol during anesthesia induction period on morbidly obese patients.
This study aims to determine the pharmacodynamics (PD) effect (measured by cardiovascular depression) of propofol during anesthesia induction period on morbidly obese (MO) patients. Four hemodynamics indexes [i.e., three indexes about blood pressure and cardiac output (CO)] representing cardiovascular function were measured. Pharmacokinetic/pharmacodynamic (PK/PD) modeling was performed by population analysis to obtain PD parameters. ⋯ In addition, the propofol EC50 value was significantly decreased in MO patients, whereas all other PD parameters were similar between control and MO subjects. This change indicated that propofol potency and/or sensitivity was increased in MO subjects. For MO patients, dosing of propofol based on LBW rather than TBW would be a safer choice due to a less cardiovascular depression effect.
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Biomed. Pharmacother. · Oct 2018
Inhibition of SETD7 protects cardiomyocytes against hypoxia/reoxygenation-induced injury through regulating Keap1/Nrf2 signaling.
The protein SET domain-containing lysine methyltransferase 7 (SETD7) has recently been shown to regulate apoptosis in various cells. However, the role of SETD7 on cardiomyocyte apoptosis during myocardial ischemia/reperfusion injury remains unclear. This study aimed to investigate the potential role of SETD7 in hypoxia/reoxygenation (H/R)-induced apoptosis of rat cardiomyocytes and reveal the underlying mechanism. ⋯ In addition, the knockdown of SETD7 increased the activity of antioxidant response element and promoted the expression of heme oxygenase-1 and NADPH-quinone oxidoreductase 1. However, the knockdown of Nrf2 partially abrogated the SETD7 inhibition-mediated protective effect against H/R injury. Taken together, these results indicate that the inhibition of SETD7 attenuates H/R-induced injury of cardiomyocytes via the down-regulation of Keap1 and promotion of the Nrf2-mediated anti-oxidation signaling pathway.