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Science China(Life Sciences) 2004年第4期47卷 303-312页

作者： Steven J. NEILL Centre for Research in Plant Science University of the West of England Bristol Coldharbour Lane Bristol BS16 1QY United Kingdom

Chitosan (CHN) specially induced the activities of 39 kD and 42 kD protein kinases in ginseng cells, which could be suppressed by an inhibitor of mitogen-activated protein kinase (MAPK) pathway, PD98059. The immunoprecipitation (IP) using MAPK antibody or kinase assay in vitro also showed that CHN-induced 42 kD and 39 kD protein kinases belonged to the MAPK family. PD98059 suppressed CHN-induced transcriptions of ginseng squalene synthase and ginseng squalene epoxidase genes (gss and gse), CHN-induced accumulation of β-Amyrin synthase (β-AS) and synthesis of saponin. These results showed that CHN-induced activities of MAPKs were necessary for the CHN-induced saponin synthesis. EGTA and LaCl3 suppressed CHN-induced 39 kD and 42 kD MAPK activities. Ruthenium red (RR) could suppress CHN-induced 39 kD activity. All of them suppressed CHN-induced saponin synthesis. These results indicated that CHN-induced increment of cytosolic calcium was necessary for CHN-induced saponin synthesis. PD98059 also suppressed CHN-induced oxidative burst (including the increment of activity of plasma membrane NADPH oxidase and production of H2O2), but diphenylene iodonium (DPI), dimethylthiourea (DMTU) and 2,5-dihydroxycinnamic acid methyl ester (DHC) could not suppress CHN-induced MAPK activities, which indicated that MAPK was possibly function upstream of CHN-induced oxidative burst. Keywords mitogen-activated protein kinase - chitosan - saponin

关键词： mitogen-activated protein kinase,chitosan,saponin.

mitogen-activated Protein Kinase Pathways Following Traumatic Brain Injury

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Neuroscience & Medicine 2011年第3期2卷 208-216页

作者： Naoki Otani Hiroshi Nawashiro Kimihiro Nagatani Satoru Takeuchi Hiroaki Kobayashi Katsuji Shima 不详

The mechanisms underlying the secondary or delayed cell death in the hippocampus and cerebral hemisphere after traumatic brain injury (TBI) have been poorly understood. Recent data suggesting that TBI may have relationship with both an inflammatory and a neurodegenerative factors are also presented. mitogen-activated protein kinases (MAPK), which play a crucial role in signal transduction, are activated by phosphorylation in response to a variety of mitogenic signals. In this article, we review the clinical and experimental evidence for brain damage after TBI. In addition, the MAPK pathways, closely involved in signal transduction after TBI, which could therefore be a new and potentially effective therapeutic target in TBI. Further investigations are therefore necessary to better understand cerebral traumatic damage and delineate the best practice strategies needed to improve the patient outcomes after TBI.

关键词： Traumatic Brain Injury mitogen-activated Protein Kinase Cell Signaling

mitogen-activated protein kinase signaling pathway and invasion and metastasis of gastric cancer

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World Journal of Gastroenterology 2015年第41期21卷 11673-11679页

作者： Mei Yang Chang-Zhi Huang Department of Etiology and Carcinogenesis & State Key Laboratory of Molecular Oncology Cancer Institute and Hospital Chinese Academy of Medical Sciences and Peking Union Medical College

The mortality rate of gastric cancer worldwide is as high as 70%, despite the development of novel therapeutic strategies. One reason for the high mortality is the rapid and uninhibited spread of the disease, such that the majority of patients are diagnosed at a stage when efficient therapeutic treatment is not available. Therefore, in-depth research is needed to investigate the mechanism of gastric cancer metastasis and invasion to improve outcomes and provide biomarkers for early diagnosis. The mitogen-activated protein kinase(MAPK) signaling pathway is widely expressed in multicellular organisms, with critical roles in multiple biological processes, such as cell proliferation, death, differentiation, migration, and invasion. The MAPK pathway typically responds to extracellular stimulation. However, the MAPK pathway is often involved in the occurrence and progression of cancer when abnormally regulated. Many studies have researched the relationship between the MAPK signaling pathway and cancer metastasis and invasion, but little is known about the important roles that the MAPK signaling pathway plays in gastric cancer. Based on an analysis of published data, this review aims to summarize the important role that the MAP kinases play in the invasion and metastasis of gastric cancer and attempts to provide potential directions for further research and clinical treatment.

关键词： mitogen-activated protein kinase Gastric cancer Si

Physiological roles of mitogen-activated-protein-kinase-activated p38-regulated/activated protein kinase

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World Journal of Biological Chemistry 2011年第5期2卷 73-89页

作者： Sergiy Kostenko Gianina Dumitriu Kari Jenssen Lgreid Ugo Moens Faculty of Health Sciences Institute of Medical BiologyUniversity of TromsφNO-9037 TromsφNorway

mitogen-activated protein kinases(MAPKs)are a family of proteins that constitute signaling pathways involved in processes that control gene expression,cell division, cell survival,apoptosis,metabolism,differentiation and *** MAPK pathways can be divided into conventional and atypical MAPK *** first group converts a signal into a cellular response through a relay of three consecutive phosphorylation events exerted by MAPK kinase kinases,MAPK kinase,and *** MAPK pathways are not organized into this three-tiered *** that belongs to both conventional and atypical MAPK pathways can phosphorylate both non-protein kinase substrates and other protein *** latter are referred to as MAPK-activated protein *** review focuses on one such MAPK-activated protein kinase,MAPK-activated protein kinase 5(MK5)or p38-regulated/activated protein kinase(PRAK).This protein is highly conserved throughout the animal kingdom and seems to be the target of both conventional and atypical MAPK *** findings on the regulation of the activity and subcellular localization,bona fide interaction partners and physiological roles of MK5/PRAK are discussed.

关键词： mitogen-activated protein kinase p38- regulated/activated protein kinase Extracellular signalregulated kinase Protein kinase A Subcellular localization Phosphorylation Protein interaction

Studies on the translocation of p38 mitogen-activated protein kinase in cardiomyocytes of nude mice on the stimulation of LPS

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Journal of Medical Colleges of PLA(China) 2000年第2期15卷 98-102页

作者：张琳姜勇张璐朴英杰赵克森

Objective: To study the translocation process of p38 mitoggen-activated protein kinase (MAPK)induced by the stimulation of lipopolysaccharide (LPS)for elucidation of the specific sighal transduction mechanism of p38 MAPK in cells Methods:Laser scanning conforal microscope and electron microscopy techniques were used to check the distribution of p38 MAPK in myocardial cells and the effect of lipopolysaccharide on its translocation Results:By the method of immunofluores- cence labeling it was found that p38spread all over the cytosol and nuclei in the quiescent or EGF stimulated cells Follow ing the stimulation of LPS for 30 min the fluorescent intensity in the nuclei of cardiomyocytes was enhanced while that in the cytosol area was reduced It was shown by electron microscope that the diffused p38 MAPK in the cytosol of the quies- cent myocardial cells moved into the nuclei following the treatment of LPS Conclusion: The stimulation fo LPS on myocardi- al cells brought about translocation of p38 MAPK into the

关键词： mitogen-activated protein kinase lipopolysaccharide translocation

Cathelicidin stimulates colonic mucus synthesis by up-regulating MUC1 and MUC2 expression through a mitogen-activated protein kinase pathway

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沈阳药科大学学报 2008年第S1期25卷 3-3页

作者： CHO Chi-hin Department of Pharmacology Chinese University of Hong Kong

Objective Mucus forms the physical barrier along the gastrointestinal(GI)*** plays an important role to prevent mucosal damage and *** previous finding showed that antibacterial peptide 'cathelicidin' increased mucus thickness and prevented inflammation in the *** the current study,we examined the protective mechanisms by which the peptide increased mucus synthesis in *** Human colonic cell line(HT-29)was used to assess the stimulatory action of cathelicidin on mucus synthesis which was measured by the D-[6-3H] glucosamine incorporation *** Human cathelicidin(LL-37)dose-dependently(10-40 μg·mL-1)and significantly stimulated mucus ***-time PCR data showed that addition of LL-37 induced more than 50% increase in MUC1 and MUC2 mRNA *** with MUC1 and MUC2 siRNAs normalized the stimulatory action of LL-37 on mucus ***-37 also activated the phosphorylation of mitogen-activated protein(MAP)kinase in the cells.A specific inhibitor of the MAP kinase pathway,U0126,completely blocked the increase of MUC1 and MUC2 expression as well as mucus synthesis by *** Taken together LL-37 stimulates mucus synthesis through the activation of MUC1 and MUC2 expression and the MAP kinase pathway in human colonic cells.

关键词： cathelicidin mucus mucin mitogen-activated protein kinase

Effect of Soothing Gan(Liver) and Invigorating Pi(Spleen) Recipes on TLR4-p38 MAPK Pathway in Kupffer Cells of Non-alcoholic Steatohepatitis Rats

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Chinese Journal of Integrative Medicine 2019年第3期25卷 216-224页

作者： GONG Xiang-wen XU Yong-jian YANG Qin-he LIANG Yin-ji ZHANG Yu-pei WANG Guan-long LI Yuan-yuan School of Chinese Medicine Jinan University

Objective: To investigate the mechanism of inflammatory-mediated toll-like receptor 4(TLR4)-p38 mitogen-activated protein kinase(p38 MAPK) pathway in Kupffer cells(KCs) of non-alcoholic steatohepatitis(NASH) rats and the intervention effect of soothing Gan(Liver) and invigorating Pi(Spleen) recipes on this pathway. Methods: After 1 week of acclimatization, 120 Sprague-Dawley male rats were randomly divided into 8 groups using a random number table(n=15 per group): normal group, model group, low-dose Chaihu Shugan Powder(柴胡疏肝散, CHSG) group(3.2 g/kg), high-dose CHSG group(9.6 g/kg), low-dose Shenling Baizhu Powder(参苓白术散, SLBZ) group(10 g/kg), high-dose SLBZ(30 g/kg) group, and low-and highdose integrated recipe(L-IR, H-IR) groups. All rats in the model and treatment groups were fed with a high-fat diet(HFD). The treatments were administrated by gastrogavage once daily and lasted for 26 weeks. The liver tissues were detected with hematoxylin-eosin(HE) and oil red O staining. Levels of liver lipids, serum lipids and transaminases were measured. KCs were isolated from the livers of rats to evaluate the mRNA expressions of TLR4 and p38 MAPK by real-time fluorescence quantitative polymerase chain reaction, and proteins expressions of TLR4, p-p38 MAPK and p38 MAPK by Western blot. Levels of inflammatory cytokines including tumor necrosis factor α(TNF-α), interleukin(IL)-1 and IL-6 in KCs were measured by enzyme-linked immunosorbent assay. Results: After 26 weeks of HFD feeding, HE and oil red O staining showed that the NASH model rats successfully reproduced typical pathogenesis and histopathological features. Compared with the normal group, the model group exhibited significant increases in body weight, liver weight, liver index, serum levels of total cholesterol(TC), triglyceride(TG), low-density lipoprotein cholesterol, and aspartate aminotransferase as well as TC and TG levels in liver tissues, and significant decrease in serum level of high-density lipoprotein choleste

关键词： non-alcoholic steatohepatitis soothing Gan (Liver)and invigorating Pi (Spleen)recipes Kupffer cel toll-like receptor 4-p38 mitogen-activated protein kinase signaling pathway inflammation,Chinese medicine

Efficacy of Lubeikangru formulation in mice with hyperplasia of the mammary glands induced by estrogen and progesterone

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Journal of Traditional Chinese Medicine 2019年第2期39卷 174-180页

作者： Sun Li Guo Donghui Liu Qian Xue Yanan Jiang Ning Zheng Hongxin Department of Basic Medicine Liaoning University of Traditional Chinese Medicine

OBJECTIVE: To evaluate the protective effects of Lubeikangru formula(LF) on hyperplasia of the mammary glands(HMG) induced by estrogen and progesterone in ***: Female mice were divided randomly into five groups: normal, model, tamoxifen(3 mg/kg),Rupixiao(900 mg/kg) and LF(900 mg/kg). All mice except those in the normal group were treated sequentially with estradiol and progesterone to induce HMG. From the tenth day of induction, mice in normal and model groups received distilled water and mice in the other groups were given the corresponding drugs by gavage, once a day, for 30 *** the end of treatment, the mammary glands, ovaries, hypothalamus, and serum was collected for whole-mount and hematoxylin and eosin(HE)staining, enzyme-linked immunosorbent assays(ELISAs), or western ***: Whole-mount and HE staining of mammary glands showed that LF rescued(at least in part) the hyperplasic morphology of the mammary glands, and the number of branch points decreased after LF treatment(P mitogen-activated protein kinase pathway.

关键词： Hyperplasia Mammary glands,animal Hormones Tamoxifen mitogen-activated protein kinases Lubeikangru formulation

Effects of Glucocorticoid?Induced Transcript 1 Gene Deficiency on Glucocorticoid Activation in Asthmatic Mice

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Chinese Medical Journal 2018年第23期131卷 2817-2826页

作者： Cheng-Ping Hu Qiu-Fen Xun Xiao-Zhao Li Xin-Yue Hu Ling Qin Ruo-Xi He Jun-Tao Feng Department of Respiratory and Critical Care Medicine Key Cite of National Clinical Research Center for Respiratory DiseaseXiangya HospitalCentral South UniversityChangshaHunan 410008China Department of Respiratory Medicine The Second Affiliated Hospital of Nanchang UniversityNanchangJiangxi 330006China Department of Nephrology Xiangya HospitalCentral South UniversityChangshaHunan 410008China

Background: Glucocorticoid (GC) is the first?line therapy for asthma, but some asthmatics are insensitive to it. Glucocorticoid?induced transcript 1 gene (GLCCI1) is reported to be associated with GCs efficiency in asthmatics, while its exact mechanism remains unknown. Methods: A total of 30 asthmatic patients received fluticasone propionate for 12 weeks. Forced expiratory volume in 1 s (FEV1) and GLCCI1 expression were detected. Asthma model was constructed in wild?type and GLCCI1 knockout (GLCCI1?/?) mice. Glucocorticoid receptor (GR) and mitogen?activated protein kinase phosphatase 1 (MKP?1) expression were detected by polymerase chain reaction and Western blotting (WB). The phosphorylation of p38 mitogen?activated protein kinase (MAPK) was also detected by WB. Results: In asthmatic patients, the change of FEV1 was well positively correlated with change of GLCCI1 expression (r = 0.430, P = 0.022). In animal experiment, GR and MKP?1 mRNA levels were significantly decreased in asthmatic mice than in control mice (wild?type: GR: 0.769 vs. 1.000, P = 0.022; MKP?1: 0.493 vs. 1.000, P < 0.001. GLCCI1?/?: GR: 0.629 vs. 1.645, P < 0.001; MKP?1: 0.377 vs. 2.146, P < 0.001). Hydroprednisone treatment significantly increased GR and MKP?1 mRNA expression levels than in asthmatic groups; however, GLCCI1?/?.asthmatic mice had less improvement (wild?type: GR: 1.517 vs. 0.769, P = 0.023; MKP?1: 1.036 vs. 0.493, P = 0.003. GLCCI1?/?: GR: 0.846 vs. 0.629, P = 0.116; MKP?1: 0.475 vs. 0.377, P = 0.388). GLCCI1?/? asthmatic mice had more obvious phosphorylation of p38 MAPK than wild?type asthmatic mice (9.060 vs. 3.484, P < 0.001). It was still higher even though after hydroprednisone treatment (6.440 vs. 2.630, P < 0.001). Conclusions: GLCCI1 deficiency in asthmatic mice inhibits the activation of GR and MKP?1 and leads to more obvious phosphorylation of p38 MAPK, leading to a decremental sensitivity to GCs.

关键词： Asthma Glucocorticoid Receptor Glucocorticoid-Induced Transcript 1 Glucocorticoids mitogen-activated Protein Kinase Phosphatase-1

Shenfu injection attenuates lipopolysaccharide-induced myocardial inflammation and apoptosis in rats

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Chinese Journal of Natural Medicines 2020年第3期18卷 226-233页

作者： CHEN Rui-Juan RUI Qing-Lin WANG Qiong TIAN Fang WU Jian KONG Xiang-Qing Cardiology Department the First Affiliated Hospital with Nanjing Medical UniversityNanjing 210029China Emergency Department Affiliated Hospital of Nanjing University of Chinese MedicineJiangsu Province Hospital of Chinese MedicineNanjing 210029China Clinical Pharmacology Department Affiliated Hospital of Nanjing University of Chinese MedicineJiangsu Province Hospital of Chinese MedicineNanjing 210029China Central Laboratory Affiliated Hospital of Nanjing University of Chinese MedicineJiangsu Province Hospital of Chinese MedicineNanjing 210029China

Shenfu injection(SFI), a Chinese medicinal product, shows potent efficacy in treating sepsis. The aim of the present study was to clarify the protective effects of SFI against lipopolysaccharide(LPS)-induced myocardial inflammation and *** were carried out in Sprague-Dawley(SD) rats treated with LPS or LPS + SFI, and in H9 C2 cardiomyocytes. The sepsisassociated myocardial inflammation and apoptosis was induced by the intraperitoneal injection of LPS(20 mg·kg–1). SFI attenuated the increased expression of tumor necrosis factor(TNF)-α and interleukin(IL)-1β induced by LPS both in serum and heart. In LPS group,cell viability was reduced, and reversed after SFI administration. LPS treatment increased the expression levels of cleaved-caspase 3 and Bax, and those of Bcl2 and Bcl2/Bax. These two trends were reversed by SFI administration. The expression levels of phosphorylated mitogen-activated protein kinase kinase(p-MEK) and phosphorylated extracellular regulated protein kinases(p-ERK) were increased by LPS, and reversed by SFI. MEK inhibitor U0126 attenuated the apoptosis induced by LPS. These results indicate that SFI could treat LPS-induced cardiac dysfunction. In conclusion, SFI attenuates the inflammation and apoptosis induced by LPS via downregulating the MEK and ERK signaling pathways.

关键词： Shenfu injection Lipopolysaccharide Inflammation Apoptosis mitogen-activated protein kinase kinase Extracellular regulated protein kinases