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International Journal of Ophthalmology(English edition) 2016年第6期9卷 799-803页

作者： Qiong Liao Yan-Ming Huang Wei Fan Chan Li Hong Yang Department of Ophthalmology Xinqiao Hospital of Third Military Medical University Department of Ophthalmology the First Affiliated Hospital of Chongqing Medical University of Chongqing Medical University Department of Ophthalmology Southwest HospitalThird Military Medical University

AIM： To clarify how the endothelial nitric oxide synthase （eNOS, NOS3） make effect on outflow facility through the trabecular meshwork （TM）. METHODS： Inhibition of NOS3 gene expression in human TM cells were conducted by three siRNAs. Then the mRNA and protein levels of NOS3 in siRNA-treated and negative control （NC） cells were determined, still were the collagen, type IV, alpha 1 （COL4A1） and fibronectin 1 by real-time PCR and Western blot analysis. In addition, NOS3 concentrations in culture supernatant fluids of TM cells were measured. Cell cycle and cell apoptosis analysis were performed using flow cytometry. RESULTS： The mRNA level of NOS3 was decreased by three different siRNA interference, similar results were obtained not only of the relative levels of NOS3 protein, but also the expression levels of COL4A1 and fibronectin 1. The number of cells in S phase was decreased, while contrary result was obtained in G2 phase. The number of apoptotic cells in siRNA-treated groups were significant increased compared to the NC samples. CONCLUSION： Abnormal NOS3 expression can make effects on the proteins levels of extracellular matrix component （e.g. fibronectin 1 and COL4A1）. Reduced NOS3 restrains the TM cell cycle progression at the G2/ M-phase transition and induced cell apoptosis.

关键词： endothelial nitric oxide synthase cell cycle cell apoptosis trabecular meshwork

Association study of the endothelial nitric oxide synthase gene polymorphisms with essential hypertension in northern Han Chinese

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Chinese Medical Journal 2006年第13期119卷 1065-1071页

作者： ZHAO Qi SU Shao-yong CHEN Shu-feng LI Biao GU Dong-feng Division of Population Genetics and Prevention Cardiovascular Institute and Fuwai Hospital Chinese Academy of Medical Sciences Peking Union Medical College Beijing 100037 China National Human Genome Center at Beijing Beijing 100176 China Institute of Biophysics Chinese Academy of Sciences Beijing100101 China

Background nitric oxide （NO） synthesized by endothelial nitric oxide synthase （eNOS） plays an important role in both the regulation of endothelial function and the control of blood pressure. Up to now, there has been conflicting data regarding the association between three clinically relevant polymorphisms （T-786C, intron4b/a and G894T） of the eNOS gene and essential hypertension.

关键词： case-control studies endothelial nitric oxide synthase haplotype hypertension single nucleotide polymorphism

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Calpa,n inhibition improves erectile function in diabetic mice via upregulating endothelial nitric oxide synthase expression and reducing apoptosis

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Asian Journal of Andrology 2018年第4期20卷 342-348页

作者： Hao Li Li-Ping Chen Tao Wang Shao-Gang Wang Ji-Hong Liu Department of Urology Tongji Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan 430030 China Institute of Urology Tongji Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan 430030 China Department of Gastroenterology Tongji Hospita Tongji Medical College Huazhong University of Science and Technology Wuhan 430030 China

Calpain activation contributes to hyperglycemia-induced endothelial dysfunction and apoptosis. This study was designed to investigate the role of calpain inhibition in improving diabetic erectile dysfunction （ED） in mice, Thirty-eight-week-old male C57BIJ6J mice were divided into three groups：（1） nondiabetic control group, （2） diabetic mice ＋ vehicle group, and （3） diabetic mice ＋ MDL28170 （an inhibitor of calpain） group. Type 1 diabetes was induced by intraperitoneal injection of streptozotocin at 60 mg kg-1 body weight for 5 consecutive days. Thirteen weeks later, diabetic mice were treated with MDL28170 or vehicle for 4 weeks. The erectile function was assessed by electrical stimulation of the cavernous nerve. Penile tissues were collected for measurement of calpain activity and the endothelial nitric oxide synthase （eNOS）-nitric oxide （NO）-cyclic guanosine monophosphate （cGMP） pathway. Terminal deoxynucleotidyl transferase 2＇-deoxyuridine 5＇-triphosphate nick end labeling （TUNEL） staining was used to evaluate apoptosis. Caspase-3 expression and activity were also measured to determine apoptosis. Our results showed that erectile function was enhanced by MDL28170 treatment in diabetic mice compared with the vehicle diabetic group. No differences in calpain-1 and calpain-2 expressions were observed among the three groups. However, caipain activity was increased in the diabetic group and reduced by MDL28170. The eNOS-NO-cGMP pathway was upregulated by MDL28170 treatment in diabetic mice. Additionally, MDL28170 could attenuate apoptosis and increase the endothelium and smooth muscle levels in corpus cavernosum. Inhibition of calpain could improve erectile function, probably by upregulating the eNOS-NO-cGMP pathway and reducing apoptosis.

关键词： apoptosis calpain diabetes endothelial nitric oxide synthase erectile dysfunction

Association of endothelial nitric oxide synthase polymorphisms with an increased risk of erectile dysfunction

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Asian Journal of Andrology 2017年第3期19卷 330-337页

作者： Lei Gao Zhifeng Zhao Fengfu Guo Yan Liu Jianhua Guo Yang Zhao Zhong Wang Department of Urinary Surgery Linyi People's Hospital Linyi 276000 China Department of Urinary Surgery Linyi Cancer Hospital Linyi 276000 China Department of Urology and Andrology Ninth People's Hospital School of Medicine Shanghai Jiao Tong University Shanghai 200011 China Department of Urology Shanghai Pudong Hospital Fudan University Pudong Medical Centre Shanghai 200011 China.

The purpose of our meta-analysis is to examine the associations between three single nucieotide polymorphisms of endothelial nitric oxide synthase （eNOS） gene, G894T, intron 4 and T-786C, and the risk of erectile dysfunction. An electronic database search was performed to identify case-control studies reporting the association between single nucleotide polymorphisms of eNOS gene and erectile dysfunction. Stringent inclusion and exclusion criteria were employed to select high-quality studies for this meta-analysis. Comprehensive Meta-analysis 2.0 software （Biostat Inc., Englewood, New Jersey, USA） was used for statistical analysis of the data extracted from the selected studies. From the initial 203 articles retrieved from database search, this meta-analysis finally selected 12 high-quality case-control studies that conformed to our inclusion criteria. The 12 studies contained a total of 1962 patients with erectile dysfunction and 1752 healthy controls. The results of our meta-analysis showed that G894T correlated with an increased risk erectile dysfunction under both the allele and dominant models （allele： OR = 1.556, 95% CI -- 1.064-2.275, P = 0.023; dominant： OR = 1.613, 95% CI = 1.050-2.476, P = 0.029）. A similar association was found between T-786C and erectile dysfunction under the allele model （OR = 1.679, 95% CI = 1.341-2.102, P 〈 0.001）, but not under the dominant model （all P 〉 0.05）. Our meta-analysis showed that the two single nucleotide polymorphisms in eNOS gene, G894T and T-786C, are strongly associated with the risk of erectile dysfunction.

关键词： endothelial nitric oxide synthase erectile dysfunction G894T intron 4 meta-analysis single nucleotide polymorphism

Up-regulation of endothelial nitric oxide synthase by cytochrome P450 arachidonic acid epoxygenase BM3F87V

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Progress in Natural Science:Materials International 2002年第8期 40-44页

作者： WANG Hong, LIN Li, LU Zaiying and WANG Daowen(Division of Cardiology, Department of Internal Medicine, Tongji Hospital, Tongji Medical College of Huazhong University of Science and Technology, Wuhan 430030, China) Division of Cardiology Department of Internal Medicine Tongji Hospital Tongji Medical College of Huazhong University of Science and Technology Wuhan 430030 China

Cytochrome P450 (CYP)-dependent metabolites of arachidonic acid, epoxyeicosatrienoic acids (EETs), have been suggested to be an endothelium-derived hyperpolarizing factor (EDHF) . However, the interaction or relation between EDHF and endothelial nitric oxide synthase (eNOS) is still to be elucidated. In the present study, the regulation of eNOS by endogenous EDHF is examined. The cytochrome P450 epoxygenase BM3F87V is cloned into the mammalian expression vector pCB6. Cultured bovine aortic endothelial cells (BAECs) less than 4 passages are used and transfected with BM3F87V. The effects of endogenous EETs result from BM3F87V transfection on eNOS are assessed in the endothelial cells by Western blot and Northern blot, and eNOS activity is also measured by the conversion of L-arginine to L-citrulline. Compared to transfection with the empty pCB6 vector, transfection of BAECs with BM3F87V significantly elevates the levels of eNOS protein expression, which is markedly inhibited by treatment with CYP inhibito

关键词： endothelium-derived hyperpolarizing factor 14 15-epoxyeicosatrienoic acid endothelial nitric oxide synthase en-dothelia] cells BM3F87V.

High-density lipoprotein regulates angiogenesis by affecting autophagy via miRNA-181a-5p

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Science China(Life Sciences) 2024年第2期67卷 286-300页

作者： Bi-Ang Kang Hua-Ming Li Ya-Ting Chen Meng-Jie Deng Yan Li Yue-Ming Peng Jian-Jun Gao Zhi-Wei Mo Jia-Guo Zhou Zhi-Jun Ou Jing-Song Ou Division of Cardiac Surgery Cardiovascular Diseases InstituteThe First Affiliated HospitalSun Yat-sen UniversityGuangzhou 510080China National-Guangdong Joint Engineering Laboratory for Diagnosis and Treatment of Vascular Diseases Guangzhou 510080China NHC key Laboratory of Assisted Circulation(Sun Yat-sen University) Guangzhou 510080China Guangdong Provincial Engineering and Technology Center for Diagnosis and Treatment of Vascular Diseases Guangzhou 510080China Division of Vascular Surgery The First Affiliated HospitalSun Yat-sen UniversityGuangzhou 510080China Department of Pharmacology Cardiac and Cerebral Vascular Research CenterZhongshan School of MedicineSun Yat-sen UniversityGuangzhou 510080China Division of Hypertension and Vascular Diseases Department of CardiologyCardiovascular Diseases InstituteThe First Affiliated HospitalSun Yat-sen UniversityGuangzhou 510080China Guangdong Provincial Key Laboratory of Brain Function and Disease Zhongshan School of MedicineSun Yat-sen UniversityGuangzhou 510080China

We previously demonstrated that normal high-density lipoprotein(nHDL)can promote angiogenesis,whereas HDL from patients with coronary artery disease(d HDL)is dysfunctional and impairs angiogenesis.Autophagy plays a critical role in angiogenesis,and HDL regulates autophagy.However,it is unclear whether n HDL and d HDL regulate angiogenesis by affecting autophagy.endothelial cells(ECs)were treated with n HDL and d HDL with or without an autophagy inhibitor.Autophagy,endothelial nitric oxide synthase(e NOS)expression,miRNA expression,nitric oxide(NO)production,superoxide anion(O2^(·-))generation,EC migration,and tube formation were evaluated.n HDL suppressed the expression of miR-181a-5p,which promotes autophagy and the expression of e NOS,resulting in NO production and the inhibition of O2^(·-)generation,and ultimately increasing in EC migration and tube formation.d HDL showed opposite effects compared to n HDL and ultimately inhibited EC migration and tube formation.We found that autophagy-related protein 5(ATG5)was a direct target of miR-181a-5p.ATG5 silencing or miR-181a-5p mimic inhibited n HDL-induced autophagy,e NOS expression,NO production,EC migration,tube formation,and enhanced O2^(·-)generation,whereas overexpression of ATG5 or miR-181a-5p inhibitor reversed the above effects of d HDL.ATG5 expression and angiogenesis were decreased in the ischemic lower limbs of hypercholesterolemic low-density lipoprotein receptor null(LDLr^(-/-))mice when compared to C57BL/6 mice.ATG5 overexpression improved angiogenesis in ischemic hypercholesterolemic LDLr^(-/-)mice.Taken together,nHDL was able to stimulate autophagy by suppressing miR-181a-5p,subsequently increasing e NOS expression,which generated NO and promoted angiogenesis.In contrast,d HDL inhibited angiogenesis,at least partially,by increasing miR-181a-5p expression,which decreased autophagy and e NOS expression,resulting in a decrease in NO production and an increase in O2^(·-)generation.Our findings reveal a novel mechanism by which HDL affects angiogenesis b

关键词： high-density lipoprotein angiogenesis autophagy ATG5 miRNA endothelial nitric oxide synthase

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The emerging role of nitric oxide in the synaptic dysfunction of vascular dementia

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Neural Regeneration Research 2025年第2期20卷 402-415页

作者： Xiaorong Zhang Zhiying Chen Yinyi Xiong Qin Zhou Ling-Qiang Zhu Dan Liu Department of Pathology Affiliated Hospital of Jiujiang UniversityJiujiangJiangxi ProvinceChina Jiujiang Clinical Precision Medicine Research Center JiujiangJiangxi ProvinceChina Center for Cognitive Science and Transdisciplinary Studies Jiujiang UniversityJiangxi ProvinceChina Department of Neurology Affiliated Hospital of Jiujiang UniversityJiujiangJiangxi ProvinceChina Department of Rehabilitation Affiliated Hospital of Jiujiang UniversityJiujiangJiangxi ProvinceChina Department of Pathophysiology School of Basic MedicineTongji Medical CollegeHuazhong University of Science and TechnologyWuhanHubei ProvinceChina

With an increase in global aging,the number of people affected by cerebrovascular diseases is also increasing,and the incidence of vascular dementia-closely related to cerebrovascular risk-is increasing at an epidemic rate.However,few therapeutic options exist that can markedly improve the cognitive impairment and prognosis of vascular dementia patients.Similarly in Alzheimer’s disease and other neurological disorders,synaptic dysfunction is recognized as the main reason for cognitive decline.nitric oxide is one of the ubiquitous gaseous cellular messengers involved in multiple physiological and pathological processes of the central nervous system.Recently,nitric oxide has been implicated in regulating synaptic plasticity and plays an important role in the pathogenesis of vascular dementia.This review introduces in detail the emerging role of nitric oxide in physiological and pathological states of vascular dementia and summarizes the diverse effects of nitric oxide on different aspects of synaptic dysfunction,neuroinflammation,oxidative stress,and blood-brain barrier dysfunction that underlie the progress of vascular dementia.Additionally,we propose that targeting the nitric oxide-sGC-cGMP pathway using certain specific approaches may provide a novel therapeutic strategy for vascular dementia.

关键词： endoplasmic reticulum stress endothelial nitric oxide synthase gene therapy nitric oxide NO-sGC-cGMP pathway synaptic dysfunction vascular dementia

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Human umbilical cord Wharton’s jelly-derived mesenchymal stem cell transplantation could improve diabetic intracavernosal pressure

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Asian Journal of Andrology 2022年第2期24卷 171-175页

作者： Jian-Hong Wu Dong-Ya Wang Lu Sheng Wei-Qing Qian Shu-Jie Xia Qi Jiang Department of Urology Shanghai General Hospital of Nanjing Medical UniversityShanghai 200080China Department of Urology Huadong Hospital Affiliated to Fudan UniversityShanghai 200040China Department of Urology Shanghai General HospitalShanghai Jiao Tong University School of MedicineShanghai 200080China

Mesenchymal stem cells(MSCs)secrete various cytokines with angiogenic and neuroprotective effects.This study aimed to assess the effects of human umbilical cord Wharton’s jelly-derived MSCs(hWJ-MSCs)on diabetes-related intracavernosal pressure(ICP)impairment in rats.hWJ-MSCs were isolated from human umbilical cord Wharton’s jelly and transplanted into the corpus cavernosum of streptozotocin(STZ)-induced diabetic rats by unilateral injection.The erectile function was evaluated at 4 weeks,as well as the expression levels of vascular endothelial growth factor(VEGF),basic fibroblast growth factor(bFGF),endothelial nitric oxide synthase(eNOS),and insulin-like growth factor 1(IGF1).STZ-induced diabetic rats showed impaired ICP,which was significantly improved by hWJ-MSC treatment.VEGF,eNOS,IGF1,and bFGF expression levels were higher in hWJ-MSC injection sites than those in control ones in STZ-induced diabetic rats.These results suggest that hWJ-MSC transplantation might improve diabetic erectile dysfunction through increased production of paracrine growth factors,highlighting a novel potential therapeutic option for erectile dysfunction.

关键词： diabetes endothelial nitric oxide synthase erectile dysfunction mesenchymal stem cells vascular endothelial growth factor

New progress in understanding roles of nitric oxide during hepatic ischemia-reperfusion injury

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World Journal of Hepatology 2022年第3期14卷 504-515页

作者： Yi-Ping Zhang Xin-Ran Liu Mei-Wen Yang Shu-Long Yang Fen-Fang Hong Experimental Center of Pathogen Biology College of MedicineNanchang UniversityNanchang 330006Jiangxi ProvinceChina Department of Surgery Fuzhou Medical CollegeNanchang UniversityFuzhou 344000Jiangxi ProvinceChina Department of Physiology College of MedicineNanchang UniversityNanchang 330006Jiangxi ProvinceChina Department of Physiology Fuzhou Medical CollegeNanchang UniversityFuzhou 344000Jiangxi ProvinceChina

Hepatic ischemia-reperfusion injury(HIRI)is a major clinical cause of morbidity and mortality in liver surgery and transplantation.Many studies have found that nitric oxide(NO)plays an important role in the HIRI and its increase or decrease can affect the progression and outcome of HIRI.However,the role of NO in HIRI is controversial and complicated.NO derived by endothelial NO synthase(eNOS)shows a protective role in HIRI,while excessive NO derived by inducible NO synthase(iNOS)accelerates inflammation and increases oxidative stress,further aggravating HIRI.Nevertheless,the overexpression of eNOS may exacerbate HIRI and iNOS-derived NO in some cases reduces HIRI.Here we review the new progress in the understanding of the roles of NO during HIRI:(1)NO possesses different roles in HIRI by increasing NO bioavailability,down-regulating leukotriene C4 synthase,inhibiting the activation of the nuclear factorκB(NFκB)pathway,enhancing cell autophagy,and reducing inflammatory cytokines and reactive oxygen species(ROS).And NO has both protective and deleterious effects by regulating apoptotic factors;(2)eNOS promotes NO production and suppresses its own overexpression,exerting a hepatoprotective effect reversely.Its activation is regulated by the PI3K/Akt and KLF2/AMPK pathways;and(3)iNOS derived NO mainly has deteriorating effects on HIRI,while it may have a protective function under some conditions.Their expression should reach a balance to reduce the adverse side and make NO protective in the treatment of HIRI.Thus,it can be inferred that NO modulating drugs may be a new direction in the treatment of HIRI or may be used as an adjunct to mitigate HIRI for the purpose of protecting the liver.

关键词： Hepatic ischemia-reperfusion injury nitric oxide endothelial nitric oxide synthase Inducible nitric oxide synthase

Anticancer activity of Δ^(9)-tetrahydrocannabinol and cannabinol in vitro and in human lung cancer xenograft

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Asian Pacific Journal of Tropical Biomedicine 2022年第8期12卷 323-332页

作者： Surang Leelawat Kawin Leelawat Thaniya Wannakup Worawan Saingam Nanthaphong Khamthong Fameera Madaka Athip Maha Patamaporn Pathompak Lukman Sueree Thanapat Songsak Medicinal Cannabis Research Institute College of PharmacyRangsit UniversityPathum Thani 12000Thailand Department of Surgery Bumrungrad International HospitalBangkok 10110Thailand Drug and Herbal Product Research and Development Center College of PharmacyRangsit UniversityPathum Thani 12000Thailand College of Oriental Medicine Rangsit UniversityPathum Thani 12000Thailand Department of Pharmacognosy College of PharmacyRangsit UniversityPathum Thani 12000Thailand

Objective:To investigate the effects of Δ^(9)-tetrahydrocannabinol,the principal psychoactive compound of Cannabis sativa,and cannabinol,a Δ^(9)-tetrahydrocannabinol degradative product,on human non-small cell lung cancer cells.Methods:Δ^(9)-Tetrahydrocannabinol and cannabinol were tested for anticancer activity in human non-small cell lung cancer(A549)cells.The effects on cell proliferation,apoptosis,and phosphorylation profiles were examined.The effects of Δ^(9)-tetrahydrocannabinol and cannabinol on tumor growth were also investigated using a xenograft nude mouse model.Apoptosis and targeted phosphorylation were verified by immunohistochemistry.Results:Δ^(9)-Tetrahydrocannabinol and cannabinol significantly inhibited cell proliferation and increased the number of apoptotic cells in a concentration-dependent manner.The Δ^(9)-tetrahydrocannabinol-and cannabinol-treated cells had lower levels of phosphorylated protein kinase B[AKT(S473)],glycogen synthase kinase 3 alpha/beta,and endothelial nitric oxide synthase compared to the controls.The study of xenograft mice revealed that tumors treated with 15 mg/kg Δ^(9)-tetrahydrocannabinol or 40 mg/kg cannabinol were significantly smaller than those of the control mice.The tumor progression rates in mice treated with 15 mg/kg Δ^(9)-tetrahydrocannabinol or 40 mg/kg cannabinol were significantly slower than in the control group.Conclusions:These findings indicate that Δ^(9)-tetrahydrocannabinol and cannabinol inhibit lung cancer cell growth by inhibiting AKT and its signaling pathways,which include glycogen synthase kinase 3 alpha/beta and endothelial nitric oxide synthase.

关键词： Cannabis Δ9-Tetrahydrocannabinol Cannabinol Non-small cell lung cancer AKT Cannabis sativa Glycogen synthase kinase 3 alpha/beta endothelial nitric oxide synthase