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Journal of Traditional Chinese Medicine 2021年第5期41卷 732-738页

作者： YAN Bin WANG Jingbo TIAN Guoqing Department of Traditional Chinese Medicine Peking Union Medical College HospitalChinese Academy of Medical SciencesBeijing 100730China

OBJECTIVE:To investigate the effect of quercetin,oleanolic acid,icariin and their compatibility on the apoptosisofhippocampalneuronsof Sprague-Dawley(SD)rats cultured with high glucose medium and the possible ***:The extracts were purchased from China Food and Drug Control Institute and *** was obtained from newborn 24 h SD *** culturing the hippocampus in different medium for 72 h,flow cytometry was used to detect the apoptosis of hippocampal neurons,and Western blot was utilized to test the expressions of p-p38,p38,p-c-Jun N-terminal kinase(JNK)and ***:Compared with the control group(CG),the neuronal apoptosis rate and the ratios of p-p38/p38 and p-JNK/JNK were significantly increased in the high glucose group(GG)(Pmitogen-activated protein kinases and JNK signaling *** the efficacy of the three drugs in combination with each other can be strengthened.

关键词： glucose hippocampus quercetin oleanolic acid icariin mitogen-activated protein kinases

Arctigenin attenuates paraquat-induced human lung epithelial A549 cell injury by suppressing ROS/p38 mitogen-activated protein kinases-mediated apoptosis

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World Journal of Emergency Medicine 2022年第5期13卷 373-378页

作者： Chao Liu Zhao-rui Sun Meng-meng Wang Zhi-zhou Yang Wei Zhang Yi Ren Xiao-qin Han Rui Liu Quan Li Shi-nan Nie Department of Emergency Medicine Jinling HospitalMedical School of Nanjing UniversityNanjing 210002China

BACKGROUND:Paraquat(PQ)-induced acute lung injury(ALI)and pulmonary fi brosis are common diseases with high mortality but without eff ective antidotes in emergency *** previous study has proved that arctigenin suppressed pulmonary fibrosis induced by *** wondered whether arctigenin could also have a protective eff ect on PQ-induced ***:A PQ-induced A549 cell injury model was used,and the effect of arctigenin was determined by a cell counting kit-8(CCK-8)cell viability *** addition,terminal deoxynucleotidyl transferase(TdT)-mediated dUTP nick-end labelling(TUNEL)staining assays and mitochondrial membrane potential assays were performed to evaluate the level of cell *** generation of reactive oxygen species(ROS)was refl ected by dihydroethidium(DHE)staining and a 2’,7’-dichlorodihy drofluorescein diacetate(DCFH-DA)***,immunoblotting studies were used to assess the expression of mitogen-activated protein kinases(MAPKs)and p38 ***:Arctigenin attenuated PQ-induced inhibition of A549 cell viability in a dose-dependent *** also significantly reduced PQ-induced A549 cell apoptosis,as refl ected by the TUNEL assay and mitochondrial membrane potential assay,which may result from suppressed ROS/p38 MAPK signaling because we found that arctigenin dramatically suppressed ROS generation and p38 MAPK ***:Arctigenin could attenuate PQ-induced lung epithelial A549 cell injury in vitro by suppressing ROS/p38 MAPK-mediated cell apoptosis,and arctigenin might be considered a potential candidate drug for PQ-induced ALI.

关键词： Paraquat A549 cells Arctigenin Reactive oxygen species mitogen-activated protein kinases Apoptosis

Effects of U0126 on growth and activation of mitogen-activated protein kinases in Aspergillus fumigatus

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Chinese Medical Journal 2013年第2期126卷 220-225页

作者： MA Dong-mei JI Ya-juan YANG Fang LIU Wei WAN Zhe LI Ruo-yu Department of Dermatology Peking University First HospitalResearch Center for Medical Mycology Peking University Beijing100034 China

Background Invasive aspergillosis （IA）, which is mainly caused by Aspergillus fumigatus （A. fumigatus）, is a major cause of morbidity and mortality in immunocompromised patients. Despite considerable progress in currently available antifungals the mortality still remains high in critically ill patients. U0126 which is a highly selective inhibitor of MEK1 and MEK2 in the RAF/MEK/ERK pathway in mammalian cells has been demonstrated to have an anti-proliferative role in cancer cells. The purpose of this study was to explore the role of U0126 on growth inhibition and activation of mitogen-activated protein kinases （MAPKs） in A. fumigatus. Methods Germination percentage and hyphae growth in A. fumigatus treated with U0126 were observed and compared with untreated controls. Western blotting analysis was used to detect changes in activation of SakA, MpkA and MpkB. Results U0126 inhibited germination and hyphae growth in A. fumigatus and enhanced the phosphorylation of SakA and MpkA under oxidative stress. U0126 at 10 pmol/L did not block the activation of MpkB during nitrogen starvation stress. Conclusion U0126 shows promise as an antifungal candidate and the MAPK pathway may be a possible antifungal drug target for A. fumigatus.

关键词： Aspergillus fumigatus protein kinase inhibitors mitogen-activated protein kinases

Ceramide induces apoptosis in human lung adenocarcinoma A549 cells through mitogen-activated protein kinases

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Acta Pharmacologica Sinica 2007年第3期28卷 439-445页

作者： Nobuo MURATA Tatsuo YAMAKAWA Department of Surgery Mini-invasive surgery CenterTeikyo University Mizonokuchi HospitalKawasaki 213-8507Japan

Aim:To provide experimental data for further research on the signal transductionof apoptosis in lung adenocarcinoma cells,we examined the effects of exogenousC2-ceramide administration on several members of the mitogen-activated proteinkinase(MAPK)superfamily and caspase-3 in A549 ***:Cell viabilityand apoptosis were analyzed by cell counting kit-8 assay and flow *** MAPK and caspase-3 proteins were detected by Western ***:C2-ceramide selectively altered the phosphorylation state &members ofthe MAPK superfamily,causing hyperphosphorylation ofmitogen-activated pro-tein kinase kinase(MEK)1/2 and the p38 MAPK,but not affecting the phosphory-lation ofextracellular signal-regulated kinase 1/2 and the c-Jun N-terminal ***-203580(a p38 MAPK inhibitor)and p38 siRNA,but not U0126(a MEKinhibitor),partially rescued cell death induced by C2-ceramide.C2-ceramide promoted theactivation of ***:Exogenous C2-ceramide induced apoptosisin human lung adenocarcinoma A549 *** activation of MAPK and caspase-3were involved in the mechanisms ofC2-ceramide-induced apoptosis in A549 cells.

关键词： ceramide apoptosis mitogen-activated protein kinases A549 cells

Evidence for a role of mitogen-activated protein kinases in the treatment of experimental acute pancreatitis

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World Journal of Gastroenterology 2014年第44期20卷 16535-16543页

作者： Natasha Irrera Alessandra Bitto Monica Interdonato Francesco Squadrito Domenica Altavilla Department of Clinical and Experimental Medicine University of Messina Department of Paediatric Gynaecological Microbiological and Biomedical Sciences University of Messina

Acute pancreatitis(AP) is an inflammatory disease characterized by acute inflammation and necrosis of the pancreatic parenchyma. AP is often associated with organ failure, sepsis, and high mortality. The pathogenesis of AP is still not well understood. In recent years several papers have highlighted the cellular and molecular events of acute pancreatitis. Pancreatitis is initiated by activation of digestive enzymes within the acinar cells that are involved in autodigestion of the gland, followed by a massive infiltration of neutrophils and macrophages and release of inflammatory mediators, responsible for the local and systemic inflammatory response. The hallmark of AP is parenchymal cell necrosis that represents the cause of the high morbidity and mortality, so that new potential therapeutic approaches are indispensable for the treatment of patients at high risk of complications. However, not all factors that determine the onset and course of the disease have been explained. Aim of this article is to review the role of mitogen-activated protein kinases in pathogenesis of acute pancreatitis.

关键词： Experimental acute pancreatitis mitogen-activated protein kinases mitogen-activated protein kinases inhibitors Cytokines Cholecystokinin Cerulein

Retinoic Aacid Diminished the Expression of MMP-2 in Hyperoxia-exposed Premature Rat Lung Fibroblasts through Regulating mitogen-activated protein kinases

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Journal of Huazhong University of Science and Technology(Medical Sciences) 2011年第2期31卷 251-257页

作者：李文斌常立文容志惠刘伟 Department of Pediatrics Tongji Hospital Tongji Medical University Huazhong University of Science and Technology

This study examined the effects of retinoic acid （RA）, PD98059, SP600125 and SB203580 on the hyperoxia-induced expression and regulation of matrix metalloproteinase-2 （MMP-2） and metalloproteinase-2 （TIMP-2） in premature rat lung fibroblasts （LFs）. LFs were exposed to hyperoxia or room air for 12 h in the presence of RA and the kinase inhibitors PD98059 （ERK1/2）, SP600125 （JNK1/2） and SB203580 （p38） respectively. The expression levels of MMP-2 and TIMP-2 mRNA were detected by semi-quantitative reverse transcription polymerase chain reaction （RT-PCR）. MMP-2 activity was measured by zymography. The amount of p-ERK1/2, REK1/2, p-JNK1/2, JNK1/2, p-p38 and p38 was determined by Western blotting. The results showed that：（1） PD98059, SP600125 and SB203580 significantly inhibited p-ERK1/2, p-JNK1/2 and p-p38 respectively in LFs; （2） The expression of MMP-2 mRNA in LFs exposed to hyperoxia was decreased after treatment with RA, SP600125 and SB203580 respectively （P0.01 or 0.05）, but did not change after treatment with PD98059 （P0.05）. Meanwhile, RA, PD98059, SP600125 and SB203580 had no effect on the expression of TIMP-2 mRNA in LFs exposed to room air or hyperoxia （P0.05）; （3） The expression of pro- and active MMP-2 experienced no change after treatment with RA or SP600125 in LFs exposed to room air （P0.05）, but decreased remarkably after hyperoxia （P0.01 or 0.05）. SB203580 inhibited the expression of pro- and active MMP-2 either in room air or under hyperoxia （P0.01）. PD98059 exerted no effect on the expression of pro- and active MMP-2 （P0.05）. It was suggested that RA had a protective effect on hyperoxia-induced lung injury by down-regulating the expression of MMP-2 through decreasing the JNK and p38 activation in hyperoxia.

关键词： hyperoxia retinoic acid lung fibroblasts premature rats matrix metalloproteinase-2 mitogen-activated protein kinases

Mechanism of Retinoic Acid and mitogen-activated protein kinases Regulating Hyperoxia Lung Injury

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Journal of Huazhong University of Science and Technology(Medical Sciences) 2006年第2期26卷 178-181页

作者：李文斌常立文容志惠张谦慎王华汪鸿刘春梅刘伟 Department of Pediatrics Tongji HospitalTongji Medical CollegeHuazhong University of Science and TechnologyWuhan 430030China

To investigate the protective effect of retinoic acid （RA） on hyperoxic lung injury and the role of RA as a modulator on mitogen-activated protein kinases （MAPKs）, gastation 21 d Sprague- Dawley （SD） fetuses （term = 22 d） were delivered by hysterotomy. Within 12-24 h of birth, premature rat pups were randomly divided into 4 groups （n= 12 each）： air-exposed control group （group Ⅰ ） ; hyperoxia-exposed group （ group Ⅱ ）, air-exposed plus RA group （group Ⅲ ）, hyperoxia-exposed plus RA group （group Ⅳ）. Group Ⅰ , Ⅲ were kept in room air, and group Ⅱ , Ⅳ were placed in 85 % oxygen. The pups in groups Ⅲ and Ⅳ were intraperitoneally injected with RA （500 μg/kg every day）. All lung tissues of premature rat pups were collected at the 4th day after birth. Terminal transferase d-UTP nick end labeling （TUNEL） staining was used for the detection of cell apoptosis. The expression of PCNA was immunohistochemically detected. Western blot analysis was employed for the determination of phosphorylated and total nonphosphorylated ERKs, JNKs or p38. Our results showed that lungs from the pups exposed to hyperoxia for 4 d exhibited TUNEL-positive nuclei increased markedly throughout the parenchyma （P〈0.01）, and decreased significantly after RA treatment （P〈0.01）. The index of PCNA-positive cells was significantly decreased （P〈0.01）, and was significantly increased by RA treatment （P〈0.01）. The air-space size was significantly enlarged, secondary crests were markedly decreased in hyperoxia-exposed animals. RA treatment improved lung air spaces and secondary crests in air-exposed pups, hut had no effect on hyperoxia-exposure pups. Western blotting showed that the amounts of JNK, p38 and ERK proteins in hyperoxia-exposure or RA-treated lung tissues were same as those in untreated lung tissues （P〈0.05）, whereas activation of these MAPKs was markedly altered by hyperoxia and RA. After hyperoxia exposure, p-ERK1/2, p-JNK1/2 and p-p38 were dramatically increased （P〈0.01）, whereas p-JNK1/2 and p

关键词： hyperoxia lung injury mitogen-activated protein kinases retinoic acid apoptosis proliferation

Tetramethylpyrazine as a potential promotion for neurogenesis in neural stem cell involved in mitogen-activated protein kinases in hypoxia disease

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Tetramethylpyrazine as a potential promotion for neurogenesi...

Antinociceptive effects of analgesic-antitumor peptide（AGAP）,a neurotoxin from the scorpion Buthus martensii Karsch on formalin-induced inflammatory pain through a mitogen-activated protein kinases-dependent Mechanism in mice

中国神经科学学会第四次会员代表大会暨第八届全国学术会议

作者： Yu-Mei TIAN,Yong LIU~*,Xin-Lin CHEN,Hai-Xia ZHANG,Jun-Feng ZHANG,Qin-Dong SHI,Peng-Bo YANG Institute of Neurobiology,Environment and Genes Related to Diseases Key Laboratory of Education Ministry,the State Key Subject for Physiology,Xi''an Jiaotong University College of Medicine

＜正＞Objective This study investigated the effects of tetramethylpyrazine（TMP）,an active element of tradional Chinese medicine Ligusticum Chuanxiong,on proliferation and differentiation of neural stem cells（NSCs） from rat brain in hypoxia condition and the activation of mitogen-activated protein kinases（MAPKs） signaling pathway during the processes. Methods we use the rat NSCs culture to investigate the effects of TMP on cell proliferation and differentiation with MTT and immunocytochemistry and western blotting analysis,and the the phosphorylation of ERK,JNK and p38 in MAPK signaling pathway was examined after TMP *** The results showed that TMP increased the proliferation and promoted the differentiation of the NSCs into *** increased the phosphorylation of ERK1/2 and decreased the phosphorylation of p38 at different *** inhibitor（U0126） in part blocked the defferetiation of the NSCs into neurons induced by *** Our findings demonstrated that TMP enhanced the proliferation and differentiation of NSCs of rat after hypoxia in vitro,in which the alteration of phosphorylation of ERK and p38 is involved.

关键词： tetramethylpyrazine neural stem cell proliferation differentiation mitogen-activated protein kinases

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Antinociceptive effects of analgesic-antitumor peptide（AGAP...

Optimized new Shengmai powder(优化新生脉散方) inhibits myocardial fibrosis in heart failure by regulating the rat sarcoma/rapidly accelerated fibrosarcoma/mitogen-activated protein kinase kinase/extracellular regulated protein kinases signaling pathway

第十一届中国生物毒素研究及医药应用年会

作者： Qing-Hong Mao Jia-Ping Ruan Wu-Guang Lu Xue-Ting Cai Juan Ye Jun-Li Cao Peng Cao Department of Anesthesiology Jiangsu Province Institute of Traditional Chinese Medicine Laboratory of Cellular and Molecular Biology Jiangsu Province Institute of Traditional Chinese Medicine Jiangsu Key Laboratory of Anesthesiology Department of AnesthesiologyAffiliated Hospital of Xuzhou Medical College

＜正＞In the present study,we investigated the anti-nociceptive effect and the underlying mechanism of the analgesic-antitumor peptide（AGAP）,a neurotoxin from the scorpion Buthus martensii *** in doses of 0.2,1 and 5 ug was intraplantar（***.） injected before formalin injection 10 min at the same *** suppression by intraplantar injection of AGAP on formalin-induced spontaneous nociceptive behaviors was *** results showed that AGAP could dose-dependent inhibit formalin-induced two-phase spontaneous flinching *** investigate the mechanism of action of treatment with AGAP in inflammatory pain,the expression of peripheral and spinal phosphorylated mitogen-activated protein kinases（phospho-MAPKs） including p-p38,p-ERK and p-JNK were *** found that formalin increased the expression of peripheral and spinal MAPKs,which were prevented by pre-intraplantar injection of AGAP in inflammation pain model in mice. Furthermore,AGAP could also decrease the expression of spinal Fos induced by formalin. The present results indicated that pre-intraplantar injection of AGAP prevented the inflammatory pain induced by formalin through a MAPKs-mediated mechanism in mice.

关键词： AGAP Formalin test mitogen-activated protein kinases c-Fos Inflammatory pain

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Journal of Traditional Chinese Medicine 2024年第3期44卷 448-457页

作者： ZHANG Zeyu JIA Zhuangzhuang SONG Yuwei ZHANG Xuan WANG Ci WANG Shuai ZHANG Peipei REN Qiuan WANG Xianliang MAO Jingyuan Department of Cardiovascular the First Teaching Hospital of Tianjin University of Traditional Chinese MedicineNational Clinical Research Center for Chinese Medicine Acupuncture and Moxibustion

OBJECTIVE: Exploring the effect of Optimized New Shengmai powder(优化新生脉散方, ONSMP) on myocardial fibrosis in heart failure(HF) based on rat sarcoma(RAS)/rapidly accelerated fibrosarcoma(RAF)/mitogen-activated protein kinase kinase(MEK)/extracellular regulated protein kinases(ERK) signaling pathway. METHODS: Randomized 70 Sprague-Dawley rats into sham(n = 10) and operation(n = 60) groups, then established the HF rat by ligating the left anterior descending branch of the coronary artery. We randomly divided the operation group rats into the model, ONSMP [including low(L), medium(M), and high(H) dose], and enalapril groups. After the 4-week drug intervention, echocardiography examines the cardiac function and calculates the ratios of the whole/left heart to the rat's body weight. Finally, we observed the degree of myocardial fibrosis by pathological sections, determined myocardium collagen(COL) Ⅰ and COL Ⅲ content by enzyme-linked immunosorbent assay, detected the m RNA levels of COL Ⅰ, COL Ⅲ, α-smooth muscle actin(α-SMA), and c-Fos proto-oncogene(c-Fos) by universal real-time, and detected the protein expression of p-RAS, p-RAF, p-MEK1/2, p-ERK1/2, p-ETS-like-1 transcription factor(p-ELK1), p-c-Fos, α-SMA, COL Ⅰ, and COL Ⅲ by Western blot. RESULTS: ONSMP can effectively improve HF rat's cardiac function, decrease cardiac organ coefficient, COL volume fraction, and COL Ⅰ/Ⅲ content, down-regulate the m RNA of COL Ⅰ/Ⅲ, α-SMA and c-Fos, and the protein of p-RAS, p-RAF, p-MEK1/2, p-ERK1/2, p-ELK1, c-Fos, COL Ⅰ/Ⅲ, and α-SMA. CONCLUSIONS: ONSMP can effectively reduce myocardial fibrosis in HF rats, and the mechanism may be related to the inhibition of the RAS/RAF/MEK/ERK signaling pathway.

关键词： extracellular regulated protein kinases heart failure mitogen-activated protein kinases myocardial fibrosis optimized new Shengmai powder rapidly accelerated fibrosarcoma sarcoma