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Effects of serum containing natural cerebrolysin on glucose-regulated protein 78 and ccaat enhancer-binding protein homologous protein expression in neuronal PC12 cells following tunicamycin-induced endoplasmic reticulum stress

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Neural Regeneration Research 2009年第2期4卷 92-97页

作者： Zhengzhi Wu Ming Li Andrew C.J. Huang O Xiuqing Jia Yinghong Li Manyin Chen Shenzhen Hospital Southern Medical University Shenzhen 518033 Guangdong Province China Larry Hiflblom Islet Research Center David Geffen School of Medicine UCLA Los Angeles CA 90024 USA

BACKGROUND： Glucose-regulated protein 78 （GRP78）, a marker of endoplasmic reticulum stress, can prolong cell survival. Alternatively, ccaat enhancer-binding protein homologous protein （CHOP）, a transcription factor specific for endoplasmic reticulum stress, can cause cell cycle arrest and cell apoptosis. OBJECTIVE： To study the protective effects of serum containing natural cerebrolysin on endoplasmic reticulum stress in tunicamycin-induced neuronal PC12 cells, and analyze the influence on GRP78 and CHOP expressions. DESIGN, TIME AND SETTING： A parallel controlled study was performed at the Institute of Integrated Western and Traditional Chinese Medicine, Shenzhen Hospital, Southern Medical University, between March 2006 and August 2008. MATERIALS： Adult Sprague-Dawley rats were perfused with natural Cerebrolysin aqueous extract （0.185 g/kg/d） to produce serum containing natural Cerebrolysin. Physiological saline was used to produce blank serum. PC12 cell line was provided by Shanghai Institute of Cell Biology, Chinese Academy of Science. Tunicamycin was provided by Sigma （St. Louis, USA）, and natural Cerebrolysin, containing ginseng, rhizoma gastrodiae, and gingko leaf （1：2：2）, by Shengzhen Institute of Integrated Western and Traditional Chinese Medicine. METHODS： PC12 cells were treated with DMEM culture media containing 10% blank serum （normal control group）, tunicamycin （1 μg/mL; model group）, and 5%, 10%, and 15% serum containing natural cerebrolysin and tunicamycin （1 μ g/mL; low-, moderate-, and high-dose serum containing natural cerebrotysin groups）, for 2 hours. MAIN OUTCOME MEASURES： PC12 cells were treated with tunicamycin for 48 hours after which apoptosis was measured using the TUNEL method to calculate apoptotic index. GRP78 expression was detected using immunocytochemistry. After 24 hours of treatment with tunicamycin, GRP78 and CHOP mRNA expressions were measured using RT-PCR. RESULTS： The apoptotic index and CHOP mRNA expression were in th

关键词： natural cerebrolysin PC12 cell strain endoplasmic reticulum stress tunicamycin glucose regulated protein 78 ccaat/enhancer-binding protein homologous protein

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Calreticulin Translocation Aggravates Endoplasmic Reticulum Stress-associated Apoptosis during Cardiomyocyte Hypoxia/Reoxygenation

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Chinese Medical Journal 2015年第3期128卷 353-360页

作者： Fei-Fei Xu Xiu-Hua Liu Department of Pathophysiology Chinese People's Liberation Army General Hospital Beijing 100853 China State Key Laboratory of Kidney Disease Chinese People's Liberation Army General Hospital Beijing 100853 China

Background： Calreticulin （CRT） is major Ca^2＋-binding chaperone mainly resident in the endoplasmic reticulum （ER） lumen. Recently, it has been shown that non-ER CRT regulates a wide array of cellular responses. We previously found that CRT was up-regulated during hypoxia/ reoxygenation （H/R） and this study was aimed to investigate whether CRT nuclear translocation aggravates ER stress （ERS）-associated apoptosis during H/R injury in neonatal rat cardiomyocytes. Methods： Apoptosis rate and lactate dehydrogenase （LDH） leakage in culture medium were measured as indices of cell injury. lmmunofluorescence staining showed the morphological changes of ER and intracellular translocation of CRT. Western blotting or reverse transcription polymerase chain reaction was used to detect the expression of target molecules. Results： Compared with control, H/R increased apoptosis rate and LDH activity. The ER became condensed and bubbled, and CRT translocated to the nucleus. Western blotting showed up-regulation of CRT, Nrf2, activating transcription factor 4 （ATF4）, CHOP and caspase-12 expression after H/R. Exogenous CRT overexpression induced by plasmid transfection before H/R increased cell apoptosis, LDH leakage, ER disorder, CRT nuclear translocation and the expression of ERS-associated molecules. However, administration of the ERS inhibitor, taurine, or CRT siRNA alleviated cell injury, ER disorder, and inhibited ERS-associated apoptosis. Conclusions： Our results indicated that during H/R stress, CRT translocation increases cell apoptosis and LDH leakage, aggravates ER disorder, up-regulates expression of nuclear transcription factors, Nrf2 and ATF4, and activates ERS-associated apoptosis.

关键词： Apoptosis Calreticulin ccaat/enhancer-binding protein homologous protein Endoplasmic Reticulum Hypoxia/Reoxygenation

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Yinchenhao decoction attenuates obstructive jaundice-induced liver injury and hepatocyte apoptosis by suppressing protein kinase RNA-like endoplasmic reticulum kinase-induced pathway

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World Journal of Gastroenterology 2019年第41期25卷 6205-6221页

作者： Yan-Li Wu Zhong-Lian Li Xi-Bo Zhang Hao Liu Graduate School of Tianjin Medical University Tianjin 300070China Department of Hepatobiliary and Pancreatic Surgery Tianjin Nankai HospitalTianjin 300100China

BACKGROUND Chronic biliary obstruction results in ischemia and hypoxia of hepatocytes,and leads to *** is very important in regulating the homeostasis of the hepatobiliary *** reticulum(ER)stress is one of the signaling pathways that induce ***,the protein kinase RNA-like endoplasmic reticulum kinase(PERK)-induced apoptotic pathway is the main way;but its role in liver injury remains *** decoction(YCHD)is a traditional Chinese medicine formula that alleviates liver injury and apoptosis,yet its mechanism is *** undertook this study to investigate the effects of YCHD on the expression of ER stress proteins and hepatocyte apoptosis in rats with obstructive jaundice(OJ).AIM To investigate whether YCHD can attenuate OJ-induced liver injury and hepatocyte apoptosis by inhibiting the PERK-ccaat/enhancer-binding protein homologous protein(CHOP)-growth arrest and DNA damage-inducible protein 34(GADD34)pathway and B cell lymphoma/leukemia-2 related X protein(Bax)/B cell lymphoma/leukemia-2(Bcl-2)*** For in vivo experiments,30 rats were divided into three groups:control group,OJ model group,and YCHD-treated *** was collected to detect the indicators of liver function,and liver tissues were used for histological *** in vitro experiments,30 rats were divided into three groups:G1,G2,and *** rats in group G1 had their bile duct exposed without ligation,the rats in group G2 underwent total bile duct ligation,and the rats in group G3 were given a gavage of *** to the serum pharmacology,serum was extracted and centrifuged from the rat blood to cultivate the BRL-3A *** deoxynucleotidyl transferase mediated dUTP nick end-labelling(TUNEL)assay was used to detect BRL-3A hepatocyte *** aminotransferase(ALT)and aspartate transaminase(AST)levels in the medium were *** blot and quantitative real-time polymerase chain reaction(qRT-PCR)analyses were

关键词： Yinchenhao decoction Obstructive jaundice Liver injury Apoptosis protein kinase RNA-like endoplasmic reticulum kinase ccaat/enhancer-binding protein homologous protein Growth arrest and DNA damage-inducible protein 34 B cell lymphoma/leukemia-2 gene B cell lymphoma/leukemia-2 gene related Ⅹ protein

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Nuclear-translocation of calreticulin aggravates endoplasmic reticulum stress-associated apoptosis during cardiomyocyte hypoxia/reoxygenation

Nuclear-translocation of calreticulin aggravates endoplasmic...

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中国生理学会第24届全国会员代表大会暨生理学学术大会

作者：徐菲菲刘秀华中国人民解放军总医院病理生理学研究室

Calreticulin（CRT）is a major Ca2+-binding chaperone mainly resident in the endoplasmic reticulum（ER）***,it has been shown that non-ER CRT regulates a wide array of cellular *** found that CRT was up-regulated during cardiomyocyte hypoxia/reoxygenation（H/R）and aimed to investigate whether CRT translocation from the ER to the nucleus aggravates ER stress-associated apoptosis during H/R in neonatal rat *** with control,H/R induced cell apoptosis and lactate dehydrogenase（LDH）*** staining showed that the ER became condensed and *** staining showed that the nuclear translocation of CRT increased significantly after H/*** blot results confirmed that H/R upregulated the nuclear expression of CRT,transcription factors,such as Nrf2 and ATF4,and markers of ER stress-associated apoptosis,such as CHOP and *** CRT overexpression induced by plasmid transfection aggravated cardiac H/R injury and ER structural *** nuclear translocation of CRT and the activation of ER stress-associated apoptosis further *** ER stress inhibitor,taurine,and CRT si RNA interference alleviated cell injury,ER damage,and inhibited ER stress-associated *** results indicated that during H/R stress,CRT translocation damages the ER structure,aggravates cell apoptosis and LDH leakage,promotes the nuclear expression of ER stress-associated transcription factors such as Nrf2 and ATF4,and activates ER stress-associated apoptosis.

关键词： calreticulin hypoxia/reoxygenation endoplasmic reticulum ccaat/enhancer-binding protein homologous protein apoptosis

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