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| 1 | The role of Rho/Rho-kinase pathway and the neuroprotective effects of fasudil in chronic cerebral ischemia显示文摘The Rho/Rho-kinase signaling pathway plays an important role in cerebral ischemia/reperfusion injury. However, very few studies have examined in detail the changes in the Rho/Rho-kinase signaling pathway in chronic cerebral ischemia. In this study, rat models of chronic cerebral ischemia were established by permanent bilateral common carotid artery occlusion and intragastrically administered 9 mg/kg fasudil, a powerful ROCK inhibitor, for 9 weeks. Morris water maze results showed that cognitive impairment progressively worsened as the cerebral ischemia proceeded. Immunohistochemistry, semi-quantitative RT-PCR and western blot analysis showed that the expression levels of Rho-kinase, its substrate myosin-binding subunit, and its related protein alpha smooth muscle actin, significantly increased after chronic cerebral ischemia. TUNEL staining showed that chronic cerebral ischemia could lead to an increase in neuronal apoptosis, as well as the expression level of caspase-3 in the frontal cortex of rats subjected to chronic cerebral ischemia. Fasudil treatment alleviated the cognitive impairment in rats with chronic cerebral ischemia, and decreased the expression level of Rho-kinase, myosin-binding subunit and alpha smooth muscle actin. Furthermore, fasudil could regulate cerebral injury by reducing cell apoptosis and decreasing caspase-3 expression in the frontal cortex. These findings demonstrate that fasudil can protect against cognitive impairment induced by chronic cerebral ischemia via the Rho/Rho-kinase signaling pathway and anti-apoptosis mechanism. | Ya-yun Yan Xiao-ming Wang Yan Jiang Han Chen Jin-ting He Jing Mang Yan-kun Shao Zhong-xin Xu | 2015 | Neural Regeneration Research2015，10，9： | 11 |
| 2 | Neuroprotective effects of Activin A on endoplasmic reticulum stress-mediated apoptotic and autophagic PC12 cell death显示文摘Activin A, a member of the transforming growth factor-beta superfamily, plays a neuroprotective role in multiple neurological diseases. Endoplasmic reticulum(ER) stress-mediated apoptotic and autophagic cell death is implicated in a wide range of diseases, including cerebral ischemia and neurodegenerative diseases. Thapsigargin was used to induce PC12 cell death, and Activin A was used for intervention. Our results showed that Activin A significantly inhibited morphological changes in thapsigargin-induced apoptotic cells, and the expression of apoptosis-associated proteins [cleaved-caspase-12, C/EBP homologous protein(CHOP) and cleaved-caspase-3] and biomarkers of autophagy(Beclin-1 and light chain 3), and downregulated the expression of thapsigargin-induced ER stress-associated proteins [inositol requiring enzyme-1(IRE1), tumor necrosis factor receptor-associated factor 2(TRAF2), apoptosis signal-regulating kinase 1(ASK1), c-Jun N-terminal kinase(JNK) and p38]. The inhibition of thapsigargin-induced cell death was concentration-dependent. These findings suggest that administration of Activin A protects PC12 cells against ER stress-mediated apoptotic and autophagic cell death by inhibiting the activation of the IRE1-TRAF2-ASK1-JNK/p38 cascade. | Long-xing Xue Hong-yu Liu Yang Cui Yue Dong Jiao-qi Wang Qiu-ye Ji Jin-ting He Min Yao Ying-ying Wang Yan-kun Shao Jing Mang Zhong-xin Xu | 2017 | Neural Regeneration Research2017，12，5： | 7 |
| 3 | Activin A prevents neuron-like PC12 cell apoptosis after oxygen-glucose deprivation显示文摘In this study, PC12 cells were induced to differentiate into neuron-like cells using nerve growth facto and were subjected to oxygen-glucose deprivation. Cells were treated with 0, 10, 20, 30, 50, 100 ng/mL exogenous Activin A. The 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl tetrazolium bromide assay and Hoechst 33324 staining showed that the survival percentage of PC12 cells significantly decreased and the rate of apoptosis significantly increased after oxygen-glucose deprivation. Exogenous Activin A significantly increased the survival percentage of PC12 cells in a dose-dependent manner. Reverse transcription-PCR results revealed a significant increase in Activin receptor IIA, Smad3 and Smad4 mRNA levels, which are key sites in the Activin A/Smads signaling pathway, in neuron-like cells subjected to oxygen-glucose deprivation, while mRNA expression of the apoptosis-regulation gene caspase-3 decreased. Our experimental findings indicate that exogenous Activin A plays an anti-apoptotic role and protects neurons by means of activating the Activin A/Smads signaling pathway. | Guihua Xu Jinting He Hongliang Guo Chunli Mei Jiaoqi Wang Zhongshu Li Han Chen Jing Mang Hong Yang Zhongxin Xu | 2013 | Neural Regeneration Research2013，8，11： | 5 |
| 4 | Changes of hypoxia-inducible factor-1 signaling and the effect of cilostazol in chronic cerebral ischemia显示文摘Hypoxia-inducible factor-1 and its specific target gene heme oxygenase-1, are involved in acute cerebral ischemia. However, very few studies have examined in detail the changes in the hypoxia-inducible factor-1/heme oxygenase-1 signaling pathway in chronic cerebral ischemia. In this study, a rat model of chronic cerebral ischemia was established by permanent bilateral common carotid artery occlusion, and these rats were treated with intragastric cilostazol (30 mg/kg) for 9 weeks. Morris water maze results showed that cognitive impairment gradually worsened as the cerebral ischemia proceeded. Immunohistochemistry, semi-quantitative PCR and western blot analysis showed that hypoxia-inducible factor-1α and heme oxygenase-1 expression levels increased after chronic cerebral ischemia, with hypoxia-inducible factor-1α expression peaking at 3 weeks and heme oxygenase-1 expression peaking at 6 weeks. These results suggest that the elevated levels of hypoxia-inducible factor-1α may upregulate heme oxygenase-1 expression following chronic cerebral ischemia and that the hypoxia-inducible factor-1/heme oxygenase-1 signaling pathway is involved in the development of cognitive impairment induced by chronic cerebral ischemia. Cilostazol treatment alleviated the cognitive impairment in rats with chronic cerebral ischemia, decreased hypoxia-inducible factor-1α and heme oxygenase-1 expression levels, and reduced apoptosis in the frontal cortex. These findings demonstrate that cilostazol can protect against cognitive impairment induced by chronic cerebral ischemic injury through an anti-apoptotic mechanism. | Han Chen Aixuan Wei Jinting He Ming Yu Jing Mang Zhongxin Xu | 2013 | Neural Regeneration Research2013，8，19： | 5 |
| 5 | Relationship of gelatinases-tight junction proteins and blood-brain barrier permeability in the early stage of cerebral ischemia and reperfusion显示文摘Gelatinases matrix metalloproteinase-2 and matrix metalloproteinase-9 have been shown to mediate claudin-5 and occludin degradation, and play an important regulatory role in blood-brain barrier permeability. This study established a rat model of 1.5-hour middle cerebral artery occlusion with reperfusion. Protein expression levels of claudin-5 and occludin gradually decreased in the early stage of reperfusion, which corresponded to the increase of the gelatinolytic activity of matrix metalloproteinase-2 and matrix metalloproteinase-9. In addition, rats that received treatment with matrix metalloproteinase inhibitor N-[(2R)-2-(hydroxamidocarbonylmethyl)-4-methylpenthanoyl]-L- tryptophan methylamide (GM6001) showed a significant reduction in Evans blue leakage and an inhibition of claudin-5 and occludin protein degradation in striatal tissue. These data indicate that matrix metalloproteinase-2 and matrix metalloproteinase-9-mediated claudin-5 and occludin degradation is an important reason for blood-brain barrier leakage in the early stage of reperfusion. The leakage of the blood-brain barrier was present due to gelatinases-mediated degradation of claudin-5 and occludin proteins. We hypothesized that the timely closure of the structural component of the blood-brain barrier (tight junction proteins) is of importance. | Haolin Xin Wenzhao Liang Jing Mang Lina Lin Na Guo Feng Zhang Zhongxin Xu | 2012 | Neural Regeneration Research2012，7，31： | 4 |
| 6 | A More Efficient Synthetic Route to Perylene-porphyrin Arrays显示文摘We present an efficient synthetic route towards two kinds of perylene-porphyrin arrays. Starting from 5, 10, 15, 20-meso-tetraphenylporphyrin, two novel 9a and 9b were designed and synthesized with 40.3% and 35.1% yield, respectively. | Xin Guo YANG, Jing Zhi SUN, Mang WANG*, Hong Zheng CHEN Department of Polymer Science & Engineering, State Key Laboratory for Silicon Materials, Zhejiang University, Hangzhou 310027 | 2003 | Chinese Chemical Letters2003，14，11： | 3 |
| 7 | The effects of repeated propofol anesthesia on spatial memory and long-term potentiation in infant rats under hypoxic conditions显示文摘Propofol is widely used as an intravenous drug for induction and maintenance in general anesthesia.Hypoxemia is a common complication during perianesthesia.We want to know the effect of propofol on spatial memory and LTP(Long-term potentiation)under hypoxic conditions.In this study,84 seven-day-old SpragueeDawley rats were randomly assigned into six groups(n Z 14)-four control groups:lipid emulsion solvent t 50%oxygen(CO),lipid emulsion solvent t room air(CA),lipid emulsion solvent t 18%oxygen(CH),and propofol t 50%oxygen(propofoleoxygen,PO);and two experiment groups:propofol t room air(propofol eair,PA),and propofol t 18%oxygen(propofolehypoxia,PH).After receiving propofol(50 mg/kg)or the same volume of intralipid intraperitoneal(5.0 ml/kg),injected once per day for seven consecutive days,the rats were exposed to 18%oxygen,50%oxygen and air,until recovery of the righting reflex.We found that the apoptotic index and activated caspase-3 increased in the PH group(P<0.05)compared with the PA group,fEPSP(field excitatory postsynaptic)potential and success induction rate of LTP reduced in all propofol groups(P<0.05).Compared with the PO group,the fEPSP and success induction rate of LTP reduced significantly in the PA and PH groups(P<0.05).Moreover,compared with CH group,the average time of escape latency was longer,and the number of platform location crossings was significantly reduced in the PH group(P<0.05).Thus,we believe that adequate oxygen is very important during propofol anesthesia. | Mang Sun Ruixue Yuan Hui Liu Jing Zhang Shengfen Tu | 2020 | Genes & Diseases2020，7，2： | 2 |
| 8 | Neuroprotective Effects of Exogenous Activin A on Oxygen-Glucose Deprivation in PC12 Cells显示文摘 | He Jin Ting Mang Jing Mei Chun-Li | 2011 | Molecules2011，17，1： | 1 |
| 9 | Nerve growth factor (NGF) combined with oxygen glucose deprivation OGD induces neural ischemia tolerance in PC12 cells 显示文摘 | Mei Chunqi He Jin-ting Mang Jing | 2011 | African Journal of Bi- ochemistry Research2011，5，10： | 1 |
| 10 | A new family of dendtimers with naphtha-line core and triphenylamine branching as a two-photon polymerization initiator 显示文摘 | Mang X M Jing F Chen Z G et al | 2011 | J Phys Chem C2011，115，： | 1 |
| 11 | Neuroproteetive Effects of Exogenous Activin A on Oxygen-Glucose Deprivation in PC12 Cells 显示文摘 | He Jin-Ting Mang Jing Mei Chun-Li | 2011 | Molecules2011，17，1： | 1 |
| 12 | NGF combined with OGD induces neural ischemia tolerance in PC12 cells 显示文摘 | Chunli Mei Jing Mang Zhongxin Xu | 2011 | African Journal of Biochemistry Researc2011，5，9： | 1 |
| 13 | Effects of SARA on Oxygen–Glucose Deprivation in PC12 Cell Line显示文摘 | Jiao-Qi Wang Jin-Ting He Zhen-Wu Du Zong-Shu Li Yong-Feng Liu Jing Mang Zhong-Xin Xu | 2013 | Neurochemical Research2013，，5： | 1 |
| 14 | Wildlife-borne microorganisms and strategies to prevent and control emerging infectious diseases显示文摘China is one of the countries with the richest wildlife population.The large variety of widely distributed species act as natural or susceptible hosts for numerous infectious diseases.It is estimated that there are more than 1.2 million unknown virus species in China,and there might be 10,000–30,000 unknown bacteria in wild mammals on the Qinghai-Tibet Plateau alone.There are no less than 600,000 species of animal-borne parasites and approximately 2 million species of fungi worldwide.With rapid economic growth and globalization,humans and wildlife interact more frequently,which enhances the probability of wildlife-borne pathogens infecting humans.The occurrence of animal-borne infectious diseases will become the“new normal”we have to face in the future.Therefore,research should be carried out on wildlife-borne microorganisms and the prevention and control of emerging infectious diseases to establish an analytical framework and an evaluation technology system for risk assessment and early warning of potential animal-borne emerging infectious diseases.This will not only improve our understanding of wildlife-borne microbial communities but also enable in-depth analysis,discovery,early warning,and even prediction of major animal-borne emerging infectious diseases that might occur in the future.Furthermore,this research will reduce response times,minimize the social and economic impact and losses,enable interventions related to the emergence or spread of the disease as early as possible,and comprehensively improve our management of infectious disease outbreaks. | Tian Qin Xiangdong Ruan Zhaojun Duan Jianping Cao Junrong Liang Jing Yang Yan Jiang Mang Shi Jianguo Xu | 2021 | Journal of Biosafety and Biosecurity2021，3，2： | 1 |
| 15 | Hernandezine induces autophagic cell death in human pancreatic cancer cells via activation of the ROS/AMPK signaling pathway显示文摘Hernandezine(Her)is a bisbenzylisoquinoline alkaloid extracted from the traditional Chinese herbal medicine Thalictrum glandulosissimum.Evidence shows that Her is a natural agonist of adenosine monophosphate(AMP)-activated protein kinase(AMPK)and induces apoptosis and autophagy in tumor cells.In this study,we investigated the role of autophagy in Her-induced cell death in human pancreatic cancer cell lines.We showed that Her dose-dependently suppressed cell proliferation,promoted autophagy and induced autophagic death in pancreatic ductal adenocarcinoma(PDAC)cell lines Capan-1 and SW1990.The IC_(50) values of Her in inhibition of Capan-1 and SW1990 cells were 47.7μM and 40.1μM,respectively.Immunoblotting showed that Her(1−40μM)promoted the conversion of LC3-I to LC3-II,and Her exerted concentration-dependent and time-dependent effects on autophagy activation in PDAC cells.In transmission electron microscopy and fluorescence image analysis,we found that autophagic vacuoles were significantly increased in Her-treated cells.Knockdown of ATG5,a key gene in the autophagy pathway,alleviated the activation of autophagy by Her.These results demonstrated that Her induced autophagy in PDAC cells.Intensely activated autophagy could promote cell death.The autophagy inhibitors,BafA1 and HCQ significantly inhibited Her-induced cell death,implying that Her induced autophagic cell death in PDAC cells.Moreover,we showed that Her activated autophagy by increasing the phosphorylation of AMPK and decreasing the phosphorylation of mTOR/p70S6K.Knockdown of AMPKαrelieves the autophagic cell death induced by Her.Furthermore,Her concentration-dependently enhanced reactive oxygen species(ROS)generation in PDAC cells.Antioxidants could reduce the phosphorylation of AMPK and suppress autophagic cell death induced by Her.Our study provides evidence for the development of Her as a therapeutic agent for the treatment of pancreatic cancer. | Chang-feng Song Yu-heng Hu Zhi-guo Mang Zeng Ye Hai-di Chen De-sheng Jing Gui-xiong Fan Shun-rong Ji Xian-jun Yu Xiao-wu Xu Yi Qin | 2023 | Acta Pharmacologica Sinica2023，44，4： | 1 |
| 16 | Effects of SARA on Oxygen–Glucose Deprivation in PC12 Cell Line显示文摘 | Jiao-Qi Wang Jin-Ting He Zhen-Wu Du Zong-Shu Li Yong-Feng Liu Jing Mang Zhong-Xin Xu | 2013 | Neurochemical Research2013，，5： | 1 |
| 17 | Use of RNAi silencing to target preconditioned glial cell line-derived neurotrophic factor in neuronal apoptosis显示文摘Several studies have suggested that exogenous glial cell line-derived neurotrophic factor may pro-tect neurons from cerebral ischemic injury. However, the mechanisms underlying the neuroprotec-tive effects of endogenous glial cell line-derived neurotrophic factor remain unclear. The present experiments sought to elucidate the influence of various conditioned media on neuronal apoptosis, using a normal culture medium for astrocytes, an astrocyte medium highly expressing glial cell line-derived neurotrophic factor, and an astrocyte medium in which glial cell line-derived neurotro-phic factor expression was silenced using RNAi technology. The results confirmed that the use of RNAi silencing to target pretreated glial cell line-derived neurotrophic factor expression promoted neuronal apoptosis. In addition, oxygen and glucose deprivation preconditioning was found to upregulate glial cell line-derived neurotrophic factor expression, and significantly reduce neuronal apoptosis. | Hongliang Guo Xinhua Li Jing Mang Ying Xing Jinting He Guihua Xu Shijun Yan LifengLiu Chunli Mei Zhongxin Xu | 2011 | Neural Regeneration Research2011，6，7： | 1 |
| 18 | Nerve growth factor (NGF) combined with oxygen glucose deprivation OGD induces neural ischemia tolerance in PC12 cells显示文摘 | Mei Chun-li He Jin-ting Mang Jing | | 0，，10： | 1 |
| 19 | Neuroprotective Effects of Exogenous Activin A on Oxygen-Glucose Deprivation in PC12 Cells显示文摘 | He Jin-Ting Mang Jing Mei Chun-Li | | 0，，01： | 1 |
| 20 | Association between the nasopharyngeal microbiome and metabolome in patients with COVID-19显示文摘SARS-CoV-2,the causative agent for COVID-19,infect human mainly via respiratory tract,which is heavily inhabited by local microbiota.However,the interaction between SARS-CoV-2 and nasopharyngeal microbiota,and the association with metabolome has not been well characterized.Here,metabolomic analysis of blood,urine,and nasopharyngeal swabs from a group of COVID-19 and non-COVID-19 patients,and metagenomic analysis of pharyngeal samples were used to identify the key features of COVID-19.Results showed lactic acid,L-proline,and chlorogenic acid methyl ester(CME)were significantly reduced in the sera of COVID-19 patients compared with non-COVID-19 ones.Nasopharyngeal commensal bacteria including Gemella morbillorum,Gemella haemolysans and Leptotrichia hofstadii were notably depleted in the pharynges of COVID-19 patients,while Prevotella histicola,Streptococcus sanguinis,and Veillonella dispar were relatively increased.The abundance of G.haemolysans and L.hofstadii were significantly positively associated with serum CME,which might be an anti-SARS-CoV-2 bacterial metabolite.This study provides important information to explore the linkage between nasopharyngeal microbiota and disease susceptibility.The findings were based on a very limited number of patients enrolled in this study;a larger size of cohort will be appreciated for further investigation. | Jing Liu Sheng Liu Zhao Zhang Xuejun Lee Wenxuan Wu Zhanlian Huang Ziying Lei Wenxiong Xu Dabiao Chen Xing Wu Yang Guo Liang Peng Bingliang Lin Yutian Chong Xiangyu Mou Mang Shi Ping Lan Tao Chen Wenjing Zhao Zhiliang Gao | 2021 | Synthetic and Systems Biotechnology2021，6，3： | 0 |
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