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HSP110 aggravates ischemia-reperfusion injury after liver transplantation by promoting NF-κB pathway 被引量:1
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作者 Qing-Zhi Hu zhen-rui cao +5 位作者 Wei-Xiong Zheng Min-Jie Zhao Jun-Hua Gong Cong Chen Zhong-Jun Wu Rui Tao 《Hepatobiliary & Pancreatic Diseases International》 SCIE CAS CSCD 2024年第4期344-352,共9页
Background:Ischemia-reperfusion injury(IRI)poses a significant challenge to liver transplantation(LT).The underlying mechanism primarily involves overactivation of the immune system.Heat shock protein 110(HSP110)funct... Background:Ischemia-reperfusion injury(IRI)poses a significant challenge to liver transplantation(LT).The underlying mechanism primarily involves overactivation of the immune system.Heat shock protein 110(HSP110)functions as a molecular chaperone that helps stabilize protein structures.Methods:An IRI model was established by performing LT on Sprague-Dawley rats,and HSP110 was silenced using siRNA.Hematoxylin-eosin staining,TUNEL,immunohistochemistry,ELISA and liver enzyme analysis were performed to assess IRI following LT.Western blotting and quantitative reverse transcription-polymerase chain reaction were conducted to investigate the pertinent molecular changes.Results:Our findings revealed a significant increase in the expression of HSP110 at both the mRNA and protein levels in the rat liver following LT(P<0.05).However,when rats were injected with siRNAHSP110,IRI subsequent to LT was notably reduced(P<0.05).Additionally,the levels of liver enzymes and inflammatory chemokines in rat serum were significantly reduced(P<0.05).Silencing HSP110 with siRNA resulted in a marked decrease in M1-type polarization of Kupffer cells in the liver and downregulated the NF-κB pathway in the liver(P<0.05).Conclusions:HSP110 in the liver promotes IRI after LT in rats by activating the NF-κB pathway and inducing M1-type polarization of Kupffer cells.Targeting HSP110 to prevent IRI after LT may represent a promising new approach for the treatment of LT-associated IRI. 展开更多
关键词 Ischemia-reperfusion injury Liver transplantation INFLAMMATION HSP110 Heat shock proteins NF-ΚB
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Effects of Nutrient Limitation on Pigments in Thalassiosira weissflogii and Prorocentrum donghaiense 被引量:14
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作者 Jian-Jun Hou Bang-Qin Huang +2 位作者 zhen-rui cao Ji-Xin Chen Hua-Sheng Hong 《Journal of Integrative Plant Biology》 SCIE CAS CSCD 2007年第5期686-697,共12页
The response of Prorocentrum donghaiense and Thalassiosira weissfiogii pigments under nitrate (N) and phosphate (P) limitation were studied using HPLC and in vivo fluorescence protocols in batch cultures. For P. d... The response of Prorocentrum donghaiense and Thalassiosira weissfiogii pigments under nitrate (N) and phosphate (P) limitation were studied using HPLC and in vivo fluorescence protocols in batch cultures. For P. donghaiense, the pigment ratio was kept stable under different nutrient conditions from the results of HPLC. For T. weissflogii, there was a lower ratio of chlorophyllide to Chl a during the exponential phase, but the reverse during the stationary phase. Different members of the phytoplankton had different pigments response mechanisms under nutrient limitation. From the results of in vivo fluorescence, the ratio of peridinin to Chl a for P. donghaiense increased in nutrient-free culture, while it was kept stable for nutrient-limited cultures during the exponential phase. For T. weissflogii, the ratio of fucoxanthin to Chl a for each culture increased during the exponential phase, but the ratio under N limitation was apparently lower than that for P limitation during the stationary phase. The results indicate that both pigment ratios from HPLC and in vivo fluorescence of To weissflogii were changed greatly under different nutrient conditions, which suggests that both ratios could be used as indicators of algal physiological status in different nutrient conditions. 展开更多
关键词 HPLC in vivo fluorescence nutrient limitation PIGMENTS Prorocentrum donghaiense Thalassiosira weissflogii.
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