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Chu Zhe,Liu Zuolong,Li Wei,Xu Dahai,Pang Li 대한독성 유전단백체 학회 2021 Molecular & cellular toxicology Vol.17 No.2
Background Carbon monoxide (CO) poisoning is a leading cause of morbidity and mortality worldwide. The delayed encephalopathy occurs a period after poisoning in patients without effective treatment. Simvastatin (Sim), a lipid-lowering drug, was reported to exert endothelial protective effects and inhibit inflammatory response. This research focused on the effects of Sim on delayed encephalopathy caused by CO poisoning. Objective The acute CO poisoning model was established by exposing rats to 2500 ppm CO gas for 40 min, then 3000 ppm for 30 min or until they lost consciousness. Rats in the treatment group were given Sim (20 mg/kg/day, ig.). The behavioral tests included the Morris water maze test and shuttle box. The pathological changes were evaluated by H and E staining. The inflammatory mediators were analyzed by ELISA. The expression levels of eNOS, iNOS and the NF-κB-related proteins were analyzed by Western blot. Results The results showed that Sim could alleviate CO-induced behavioral disorders and the hippocampal nerve cells apoptosis. Sim administration reversed the effects of CO on oxidative stress-related molecules. Sim could also inhibit the production of the inflammatory mediators induced by CO. The level of eNOS was decreased after CO exposure, while iNOS was increased. Sim could significantly inhibit the effects of CO. Furthermore, Sim inhibited the phosphorylation of IκBα (an NF-κB inhibitory protein), i.e., the activation of NF-κB, which indicated that Simvastatin reduced the inflammatory response induced by CO poisoning partially through inhibiting the activation of NF-κB signaling pathway. Conclusion To sum up, our research indicated that Sim could attenuate the delayed encephalopathy induced by CO poisoning via regulating oxidative stress, inflammation and NF-κB pathway. Background Carbon monoxide (CO) poisoning is a leading cause of morbidity and mortality worldwide. The delayed encephalopathy occurs a period after poisoning in patients without effective treatment. Simvastatin (Sim), a lipid-lowering drug, was reported to exert endothelial protective effects and inhibit inflammatory response. This research focused on the effects of Sim on delayed encephalopathy caused by CO poisoning. Objective The acute CO poisoning model was established by exposing rats to 2500 ppm CO gas for 40 min, then 3000 ppm for 30 min or until they lost consciousness. Rats in the treatment group were given Sim (20 mg/kg/day, ig.). The behavioral tests included the Morris water maze test and shuttle box. The pathological changes were evaluated by H and E staining. The inflammatory mediators were analyzed by ELISA. The expression levels of eNOS, iNOS and the NF-κB-related proteins were analyzed by Western blot. Results The results showed that Sim could alleviate CO-induced behavioral disorders and the hippocampal nerve cells apoptosis. Sim administration reversed the effects of CO on oxidative stress-related molecules. Sim could also inhibit the production of the inflammatory mediators induced by CO. The level of eNOS was decreased after CO exposure, while iNOS was increased. Sim could significantly inhibit the effects of CO. Furthermore, Sim inhibited the phosphorylation of IκBα (an NF-κB inhibitory protein), i.e., the activation of NF-κB, which indicated that Simvastatin reduced the inflammatory response induced by CO poisoning partially through inhibiting the activation of NF-κB signaling pathway. Conclusion To sum up, our research indicated that Sim could attenuate the delayed encephalopathy induced by CO poisoning via regulating oxidative stress, inflammation and NF-κB pathway.
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KeXin Li,DaWei Chen,XiuLi Zhao,HaiYang Hu,ChunRong Yang,DaHai Pang 대한약학회 2011 Archives of Pharmacal Research Vol.34 No.11
We prepared and optimized Ulex europaeus agglutinin I (UEAI)-modified Bovine serum albumin (BSA)-encapsulating liposomes (UEAI-LIP) as oral vaccine carriers and examined the feasibility of inducing systemic and mucosal immune responses by oral administration of UEAILIP. The prepared systems were characterized in vitro for their average size, zeta potential,encapsulation efficiency (EE%) and conjugation efficiency (CE%). In vitro release studies indicated that the presence of UEAI around the optimized liposomes was able to prevent a burst release of loaded BSA and provide sustained release of the encapsulated protein. In vivo immune-stimulating results in KM mice showed that BSA given intramuscularly generated systemic response only but both systemic and mucosal immune responses could be induced simultaneously in the groups in which BSA-loaded liposomes (LIP) and UEAI-LIP were administered intragastrically. Furthermore, the modification of UEAI on the surface of liposomes could further enhance the IgA and IgG levels obviously. In conclusion, this study demonstrated the high potential of lectin-modified liposomes containing the antigen as carriers for oral vaccine.
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