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Cerebral microvascular dysfunction and neurodegeneration in dementia

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Stroke & Vascular Neurology 2019年第2期4卷 105-107页

作者： Feng Han Key Laboratory of Cardiovascular and Cerebrovascular Medicine School of PharmacyNanjing Medical UniversityNanjingJiangsuChina

Maintaining normal learning and memory functions requires a high degree of coordination between neural and vascular cells.Basic and clinical studies have shown that brain microvasculature dysfunction activates inflammatory cells in the brain,leading to progressive neuronal loss and eventually dementia.This review focuses on recent studies aimed at identifying the molecular events that link cerebral microvascular dysfunction to neurodegeneration,including oxidative/nitrosative stress,cellular metabolic dysfunction,inflammatory signalling and abnormal synaptic plasticity.A better understanding of the coupling between vasculature and brain neurons and how this coupling is disrupted under pathological conditions is of great significance in identifying new diagnostic and treatment targets for dementia for which no new drugs have been approved since 2003.

关键词： dysfunction drugs eventually

Danggui Buxue Tang ameliorates bleomycin-induced pulmonary fibrosis in rats through inhibiting transforming growth factor-β1/Smad3/plasminogen activator inhibitor-1 signaling pathway

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Journal of Traditional Chinese medicine 2020年第2期40卷 236-244页

作者： Wang Jiepeng Fang Chaoyi Wang Shaoxian Fang Fang Chu Xinqiao Liu Na Lu Chenxi Wang Shuo Li Wei School of Preclinical medicine Hebei University of Chinese MedicineShijiazhuang 050200China Hebei Key Laboratory of Chinese medicine Research on Cardio-cerebrovascular Disease Hebei University of Chinese MedicineShijiazhuang 050091China

OBJECTIVE: To investigate the effect of Danggui Buxue Tang(DBT), a decoction from Traditional Chinese medicine, on bleomycin-induced pulmonary fibrosis in rats, and to propose the possible underlying mechanism.METHODS: Forty male Sprague-Dawley rats were randomly divided into sham group, model group,prednisone group and DBT group. Pulmonary fibrosis rat model was established by intratracheal injection with bleomycin. Body weight and lung index were monitored. Histopathologic examination and collagen deposition were determined using Hematoxylin and eosin(HE) and Masson's trichrome staining. Immunohistochemistry staining was applied to observe the expression of alpha-smooth muscle actin(α-SMA). m RNA expression of α-SMA,collagen Ⅰ and collagen Ⅲ were measured by realtime fluorescence quantitative PCR(RT-q PCR). Inflammatory cytokines, including tumor necrosis factor alpha(TNF-α), interleukin-6(IL-6) and IL-1β in serum were detected by Enzyme-linked immunosorbent assay. Alkali hydrolysis method was conducted to investigate the content of hydroxyproline(HYP). Transforming growth factor-β1(TGF-β1),Smad3 and plasminogen activator inhibitor-1(PAI-1) protein level were examined by Western blot assay.RESULTS: DBT significantly reduced the severity of bleomycin-induced pulmonary fibrosis and inflammation as indicated by minimizing the lost of weight, and by lowering the levels of lung index, inflammation score, Ashcroft score, collagen volume fraction(%), HYP, α-SMA, collagen Ⅰ, collagen Ⅲ,TNF-α, IL-6, IL-1β, TGF-β1, Smad3 and PAI-1, consistent with the effect of prednisone.CONCLUSION: Our findings suggest that DBT is able to ameliorate the pulmonary fibrosis, the possible mechanism may involve inhibition of pulmonary inflammation and collagen deposition, possibly via suppressing TGF-β1/Smad3/PAI-1 signaling pathway.

关键词： Pulmonary fibrosis Transforming growth factor beta 1 Smad3 protein Plasminogen inactivators Danggui Buxue Tang

Histamine H1 Receptor in Basal Forebrain Cholinergic Circuit:A Novel Target for the Negative Symptoms of Schizophrenia?

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Neuroscience Bulletin 2022年第5期38卷 558-560页

作者： Shuangshuang Wu Chenshu Gao Feng Han Heming Cheng Key Laboratory of Neuropharmacology and Translational medicine of Zhejiang Province School of Pharmaceutical SciencesZhejiang Chinese Medical UniversityHangzhou 310053China Key Laboratory of Cardiovascular and Cerebrovascular Medicine School of PharmacyNanjing Medical UniversityNanjing 211166China

Schizophrenia is a common and severe mental disorder with a lifetime prevalence of~1%[1]Apart from the typical positive symptoms,such as hallucinations and delusions,which mainly make patients seek medication,60%-70%of patients are tortured by negative symptoms(e.***.apathy and alogia)and cognitive deficits that impose a long-term burden on patients[2].

关键词： Schizophrenia patients medication

γ-catenin alleviates cardiac fibrosis through inhibiting phosphorylation of GSK-3β

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The Journal of Biomedical Research 2020年第1期34卷 27-35页

作者： Xin Tang Jiaxin Tian Liping Xie Yong Ji Key Laboratory of Cardiovascular and Cerebrovascular Medicine Key Laboratory of Targeted Intervention and Cardiovascular DiseaseCollaborative Innovation Center for Cardiovascular Disease Translational MedicineNanjing Medical UniversityNanjingJiangsu 211166China

Cardiac fibrosis is a common pathological change of many cardiovascular diseases. β-catenin has been shown to promote fibrosis. However, the precise role of its homolog γ-catenin in the process of fibrosis remains largely unclear. In this study, we found that the expression of γ-catenin was significantly decreased in angiotensin Ⅱ(Ang Ⅱ)-induced cardiac fibrosis model, contrary to most reports of β-catenin. Overexpression of γ-catenin in cardiac fibroblasts(CFs) significantly inhibited the expression of α-smooth muscle actin(α-SMA), whereas knocking down the expression of γ-catenin with si RNA promoted the occurrence of cardiac fibrosis.Mechanistically, γ-catenin could bind to GSK-3β to inhibit the phosphorylation of GSK-3β, therefore preventing cardiac fibrosis. Our study shows that γ-catenin is an important protective factor in cardiac fibrosis, which provides a new potential target for the treatment of cardiac fibrosis.

关键词： γ-catenin cardiac fibrosis GSK-3β

Downregulation of miR-181a-5p alleviates oxidative stress and inflammation in coronary microembolization-induced myocardial damage by directly targeting XIAP

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Journal of Geriatric Cardiology 2021年第6期18卷 426-439页

作者： You ZHOU Man-Yun LONG Zhi-Qing CHEN Jun-Wen HUANG Zhen-Bai QIN Lang LI Department of Cardiology the First Affiliated Hospital of Guangxi Medical UniversityNanningChina Guangxi Key Laboratory of Precision medicine in Cardio-cerebrovascular Diseases Control and Prevention NanningChina

BACKGROUND Coronary microembolization(CME)is a complicated problem that commonly arises in the context of coronary angioplasty.MicroRNAs play crucial roles in cardiovascular diseases.However,the role and mechanism of miR-181a-5p in CME-induced myocardial injury remains unclear.METHODS We established CME rat models.Cardiac function was detected by echocardiography.Haematoxylin-basic fuchsin-picric acid staining was used to measure micro-infarction size.Serum samples and cell culture supernatants were evaluated via enzyme-linked immunosorbent assay.Cellular reactive oxygen species were determined by dichloro-dihydro-fluorescein diacetate assay,and the other oxidative stress related parameters were assayed by spectrophotometry.The dual-luciferase reporter(DLR)assay and RNA pulldown were conducted to validate the association between miR-181a-5p and X-linked inhibitor of apoptosis protein(XIAP).The expression of miR-181a-5p and XIAP mRNA were determined by quantitative reverse transcription polymerase chain reaction.Proteins were evaluated via immunoblotting.The viability of the cell was evaluated via cell counting kit-8 assay.RESULTS The miR-181a-5p level was significantly increased in CME myocardial tissues.Downregulation of miR-181a-5p improved CME-induced cardiac dysfunction and alleviated myocardial oxidative stress and inflammatory injury,whereas miR-181a-5p exhibited the opposite effects.Then,the DLR assay and RNA pulldown results revealed that miR-181a-5p directly targeting on XIAP.The XIAP level was found to be remarkably decreased after CME.XIAP overexpression attenuated CME-induced myocardial oxidative stress and inflammatory injury.Finally,in vitro rescue experiments revealed that knockdown of XIAP could abolish the protective effects of miR-181a-5p knockdown on hypoxia-induced cardiomyocyte oxidative stress and inflammatory injury.CONCLUSIONS Downregulation of miR-181a-5p alleviates CME-induced myocardial damage by suppressing myocardial oxidative stress and inflammation through directly targeting XIAP.

关键词： damage XIAP Down

H2S protects against diabetes-accelerated atherosclerosis by preventing the activation of NLRP3 inflammasome

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The Journal of Biomedical Research 2020年第2期34卷 94-102页

作者： Qiao Zheng Lihong Pan Yong Ji Key Laboratory of Cardiovascular and Cerebrovascular Medicine Key Laboratory of Targeted Intervention of Cardiovascular DiseaseCollaborative Innovation Center for Cardiovascular Disease Translational MedicineNanjing Medical UniversityNanjingJiangsu 211166China

Hydrogen sulfide(H2S) is an important messenger for its strong anti-inflammatory effects, which may be involved in multiple cardiovascular diseases. In our previous study, we revealed that H2S attenuated diabetesaccelerated atherosclerosis through suppressing oxidative stress. Here we report that GYY4137, a H2S donor,reduced the plaque formation of aortic roots and the levels of both intercellular cell adhesion molecule 1(ICAM1)and vascular cell adhesion molecule 1(VCAM1) in diabetes-accelerated atherosclerotic cells and mouse models.The inflammatory factors of TNF-α, IL-1β, IL-6, and MCP1 were also significantly reduced by GYY4137.Mechanically, GYY4137 suppressed the activation of pyrin domain containing protein 3(NLRP3) inflammasome in diabetes-accelerated atherosclerosis conditions. Upon knockdown of NLRP3, the increase of ICAM1 and VCAM1 caused by high glucose and ox LDL could be reversed, indicating that H2S protected the endothelium by inhibiting the activity of NLRP3 inflammasome. In conclusion, our study indicates that GYY4137 effectively protects against the development of diabetes-accelerated atherosclerosis by inhibiting inflammasome activation.

关键词： H2S NLRP3 inflammation diabetes-accelerated atherosclerosis

Neurotransmitter receptors on microglia

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Stroke & Vascular Neurology 2016年第2期1卷 52-58页

作者： Huan Liu Rehana K Leak Xiaoming Hu Center of cerebrovascular Disease Research University of Pittsburgh School of MedicinePittsburghPennsylvaniaUSA Division of Pharmaceutical Sciences Duquesne UniversityPittsburghPennsylvaniaUSA

As the resident immune cells in the central nervous system,microglia have long been hypothesised to promote neuroinflammation and exacerbate neurotoxicity.However,this traditional view has undergone recent revision as evidence has accumulated that microglia exert beneficial and detrimental effects depending on activation status,polarisation phenotype and cellular context.A variety of neurotransmitter receptors are expressed on microglia and help mediate the bidirectional communication between neurons and microglia.Here we review data supporting the importance of neurotransmitter receptors on microglia,with a special emphasis on glutamate,γ-aminobutyric acid(GABA),norepinephrine,cannabinoid and acetylcholine receptors.We summarise evidence favouring a significant role for neurotransmitter receptors in modulating microglial activation,phagocytic clearance and phenotypic polarisation.Elucidating the effects of neurotransmitter receptors on microglia and dissecting the underlying mechanisms may help accelerate the discovery of novel drugs that tap the therapeutic potential of microglia.

关键词： drugs inflammation supporting

Sanhua Tang (三化汤) protects against ischemic stroke by preventing blood-brain barrier injury: A network pharmacology and in vivo experiments

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Journal of Traditional Chinese medicine 2024年

作者： LUO Shan YANG Fan CHEN Yuanchun ZHAO Ruoxi LIU Haiye GAO Fei MA Wencan GAO Weijuan YU Wentao Hebei International Joint Research Centre for Acupuncture and Moxibustion of Traditional Chinese medicine College of Basic medicine Hebei University of Chinese medicine Graduate School Hebei University of Chinese medicine College of Acupuncture and Massage Hebei University of Chinese medicine Hebei Key Laboratory of Chinese medicine Research on Cardio-cerebrovascular Diseases

OBJECTIVE: To assess the effect and mechanism of Sanhua Tang (三化汤， SHT) in treating ischemic stroke (IS) through the "Kaitong Xuanfu" theory by using network pharmacology and animal experiments. METHODS: The active ingredients and targets of SHT and IS were screened by public databases such as Traditional Chinese medicine systems pharmacology， GeneCards， and online mendelian inheritance in man. Visual network topographies were constructed using R， Cytoscape 3.6.0， AutoDockTools， a user-sponsored molecular visualization system on an open-source foundation， and other software to analyze the correlation between targets and active ingredients. The middle cerebral artery occlusion (MCAO) model was established by operation. Animals were divided into the Sham group， MCAO group (M group)， aloeemodin (AE) group (MCAO rats treated with aloe-emodin)， SHT at low dosage (SL group) (MCAO rats treated with SL)， SHT at medium dosage (SM group)， and SHT at high dosage (SH group). 2，3，5-triphenyl tetrazolium chloride staining was used to detect the volume of cerebral infarction; Nissl staining was used to observe the morphology of neuronal cells; transmission electron microscopy was used to observe the integrity of the blood-brain barrier (BBB); enzyme-linked immunosorbent assay was used to detect the content of interleukin-6 (IL-6)， IL-10， tumor necrosis factor α (TNF-α) in serum. Western blot was used to detect the expression of vascular endothelial growth factor A (VEGFA) protein in the cerebral ischemic penumbra. RESULTS: Using network pharmacology and molecular docking validation， four active ingredients (lignan， naringenin， aloe rhodopsin， and β-sitosterol)， seven target proteins [protein kinase b 1， IL-6， TNF， VEGFA， TP53， jun proto-oncogene， and cysteinyl aspartate specific proteinase 3]， and inflammatory signaling pathways were identified. Animal experiments showed that the SH and AE groups had fewer neurological deficits， reduced brain infarct volumes， decreased serum inflammatory factor levels， increased expression of

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Multiple hurdle mechanism and blood-brain barrier in epilepsy:glucocorticoid receptor-heat shock proteins on drug regulation

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Neural Regeneration Research 2021年第12期16卷 2427-2428页

作者： Aneesha Achar Chaitali Ghosh cerebrovascular Research Department of Biomedical EngineeringLerner Research InstituteCleveland ClinicClevelandOHUSA Department of Biomedical Engineering and Molecular medicine Cleveland Clinic Lerner College of Medicine of Case Western Reserve UniversityClevelandOHUSA

Epilepsy is a complex neurologic condition which affects over 50 million people worldwide.Pharmacotherapy,primarily involving the use of anti-seizure drugs(ASDs),is an essential part of controlling seizures.However,nearly 30%of patients develop drug-resistant epilepsy,clinically defined as the persistence of seizure following trials of two ASDs(Kwan et al.,2010).Although several hypotheses have been proposed to explain this phenomenon,the mechanism of drug-resistant epilepsy still remains unclear.

关键词： epilepsy drug drugs