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Fangchinoline induces antiviral response by suppressing STING degradation

JOURNAL OF PHARMACEUTICAL ANALYSIS 2024年第6期14卷 100972页

作者： Wang, Jinyong Xie, Fang Jia, Xin Wang, Xuejiao Kong, Lingdong Li, Yiying Liang, Xue Zhang, Meiqi He, Yuting feng, wandi Luo, Tong Wang, Yao Xu, Anlong Beijing Univ Chinese Med Sch Chinese Mat Med Beijing 100029 Peoples R China Beijing Univ Chinese Med Sch Life Sci Beijing 100029 Peoples R China Chinese Acad Med Sci & Peking Union Med Coll Inst Mat Med Beijing Key Lab Drug Target Identificat & New Drug Beijing 100050 Peoples R China

The stimulator of interferon genes (STING), an integral adaptor protein in the DNA-sensing pathway, plays a pivotal role in the innate immune response against infections. Additionally, it presents a valuable therapeutic target for infectious diseases and cancer. We observed that fangchinoline (Fan), a bisbenzylisoquinoline alkaloid (BBA), effectively impedes the replication of vesicular stomatitis virus (VSV), encephalomyocarditis virus (EMCV), influenza A virus (H1N1), and herpes simplex virus-1 (HSV-1) in vitro. Fan treatment significantly reduced the viral load, attenuated tissue inflammation, and improved survival in a viral sepsis mouse model. Mechanistically, Fan activates the antiviral response in a STINGdependent manner, leading to increased expression of interferon (IFN) and interferon-stimulated genes (ISGs) for potent antiviral effects in vivo and in vitro. Notably, Fan interacts with STING, preventing its degradation and thereby extending the activation of IFN-based antiviral responses. Collectively, our findings highlight the potential of Fan, which elicits antiviral immunity by suppressing STING degradation, as a promising candidate for antiviral therapy. (c) 2024 Published by Elsevier B.V. on behalf of Xi'an Jiaotong University. This is an open access article under the CC BY-NC-ND license (http://***/licenses/by-nc-nd/4.0/).

关键词： Fangchinoline Virus Type I interferons Stimulator of interferon genes Protein degradation

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丹酚酸A对OGD/R诱导脑微血管内皮细胞凋亡和氧化应激损伤的作用及机制

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中国药学杂志 2024年第10期59卷 904-910页

作者：尚宇夫刘漫刘冬妮张文芳冯丹虹徐双冯琬迪杜冠华王月华中国医学科学院药物研究所药物靶点研究与新药筛选北京市重点实验室北京100050

目的研究丹酚酸A(salvianolic acid A,SAL-A)对氧糖剥夺/复氧(oxygen-glucose deprivation/reoxygenation,OGD/R)诱导脑微血管内皮细胞(brain microvascular endothelial cells,***.3)凋亡和氧化应激损伤的作用及机制。方法应用***.3细胞OGD/R损伤模型评价SAL-A对OGD/R诱导***.3细胞凋亡和氧化应激的作用及机制。膜联蛋白V-异硫氰酸荧光素探针(Annexin V-fluorescein isothiocyanate,Annexin V-FITC)以及碘化丙啶(propidium iodide,PI)染色检测细胞凋亡;2,7-二氯荧光素二乙酸酯(2′,7′-dichlorodihydrofluorescein diacetate,DCFH-DA)探针检测细胞活性氧(reactive oxygen species,ROS)生成;JC-1染色法检测细胞线粒体膜电位;以免疫印迹法检测细胞凋亡、氧化应激及蛋白激酶B(protein kinase B,Akt)/糖原合成酶激酶-3β(glycogen synthase kinase-3β,GSK3β)/核转录因子E2相关因子(nuclear factor erythroid 2 related factor 2,Nrf2)通路相关蛋白的表达。结果与正常对照组比较,OGD/R组抗凋亡蛋白表达、线粒体膜电位水平、相关抗氧化蛋白表达、Akt/GSK3β/Nrf2通路表达均显著降低(P<0.05),而细胞凋亡数、凋亡诱导蛋白表达、细胞内ROS产生均显著增高(P<0.05);而SAL-A处理后可改善OGD/R诱导的细胞凋亡和氧化应激,Akt/GSK3β/Nrf2通路蛋白表达显著增高。结论SAL-A能够抑制OGD/R所诱导的脑微血管内皮细胞凋亡与氧化应激损伤,机制与调控Akt/GSK3β/Nrf2通路相关。

关键词：丹酚酸A 氧糖剥夺/复氧细胞凋亡氧化应激

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Mechanism of mitochondrial protection by the Buyin Qianzheng formula in a Parkin overexpression cell model

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Journal of Traditional Chinese Medical Sciences 2022年第1期9卷 59-68页

作者： Cuicui Cheng Yushan Gao Cong Gai wandi feng Haojie Ma Jing feng Zhenyu Guo Shujing Zhang Jie Wu Hongmei Sun School of Traditional Chinese Medicine Beijing University of Chinese MedicineBeijing102488China Institute of Health Sciences National Engineering Research Center for Beijing Biochip TechnologyBeijing102206China Department of Physiology Mayo Clinic HospitalPhoenix85054USA

Objective:To identify the molecular mechanisms of the effects of the Buyin Qianzheng formula(BYQZF)on the mitochondrial dynamics in a Parkin overexpression Parkinson's disease(PD)cell ***:First,a stable Parkin overexpression cell model was constructed using plasmid ***,we examined the protective effect of BYQZF on the mitochondrial dysfunction of the Parkin overexpression PD cell model induced by neurotoxin 1-methyl-4-phenylpyridinium ion(MPPþ).The mRNA expression level of Parkin was evaluated using real-time quantitative *** cell survival rate was detected using the Cell Counting Kit-8 *** evaluated the cellular adenosine triphosphate(ATP)levels using luciferase assays.A laser scanning confocal microscope was used to observe the mitochondrial morphology,activity,and mitochondrial membrane potential(DJm).Western blot was conducted to evaluate the levels of the fusion proteins mitofusin1,mitofusin2,optic atrophy 1,dynaminrelated protein 1,and mitochondrial fission protein ***:Parkin overexpression attenuated MPPþ-induced mitochondrial damage,increased mitochondrial activity and *** increased the survival of MPPþ-induced cells that overexpressed Parkin and upregulated the mitochondrial form factor and *** also inhibited a decrease in the DJm and ATP *** findings suggested that BYQZF protected against MPPþ-induced mitochondrial dysfunction and enhanced the protective effect of Parkin ***,the formula upregulated the expression of the fusion proteins mitofusin1,mitofusin2,and optic atrophy 1(closely related to mitochondrial quality remodeling),and reduced the expression of the fission protein dynamicrelated protein 1,as well as mitochondrial fission protein ***:The mechanism by which BYQZF increased the mitochondrial protective effect of Parkin gene overexpression in MPPþ-induced cells may be related to improving mitochondrial function and regulating the balance of mitochondrial

关键词： Parkinson's disease Parkin overexpression Mitochondria Buyin Qianzheng formula Neurotoxin 1-methyl-4-phenylpyridinium ion SH-SY5Y Mitofusin 2 Dynamic-related protein 1

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Combination therapy of scalp electro-acupuncture and medication for the treatment of Parkinson's disease: A systematic review and meta-analysis

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Journal of Traditional Chinese Medical Sciences 2019年第1期6卷 26-34页

作者： Tianyao Qiang Cong Gai Yuan Chai wandi feng Haojie Ma Yi Zhang Jing feng Zhenyu Guo Ling Ma Hongmei Sun School of Traditional Chinese Medicine Beijing University of Chinese MedicineBeijing 100029China Universitélibre de Bruxelles Brussels 1050Belgium

Objective:To summarize the current clinical evidence related to the therapeutic effects and safety of adjuvant scalp electro-acupuncture (SEA) treatment for Parkinson's disease in ***:Following the PRISMA statement,seven electronic databases were searched to retrieve randomized controlled clinical trials that used SEA combined with medication as the treatment intervention,and medication as the *** 5.3 was used to analyze outcomes,including the Unified Parkinson's Disease Rating Scale (UPDRS),Webster scale,effectiveness rate,and UPDRS ***:Nine randomized controlled trials,with certain methodological flaws and risks of bias,were included that involved 474 *** combined with medication was more effective than medication alone in overall therapeutic effects,as evidenced by total UPDRS scores (mean difference (MD):7.15,95% confidence interval [CI] 0.24 to 14.07,P =.04),Webster scores (MD:1.60,95% CI 0.20 to 2.99,P =.03),and effectiveness rate (risk ratio:1.35,95% CI 1.19 to 1.54,P <.001).In addition,there was significant improvement in pooled motor function results after adjuvant SEA treatment compared with medication alone (MD:5.75,95% Cl 4.18 to 7.32,P <.001).Conclusion:The combination of SEA and medication may be a promising intervention for patients with Parkinson's disease,especially to improve motor ***,results were inconclusive,and additional studies with rigorous experimental design and larger sample sizes are needed to verify these results.

关键词： Parkinson's disease Scalp electro-acupuncture Unified Parkinson's Disease Rating Scale Motor function

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Protective effects of Buyinqianzheng Formula on mitochondrial morphology by PINK1/Parkin pathway in SH-SY5Y cells induced by MPP^(+)

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Journal of Traditional Chinese Medical Sciences 2020年第3期7卷 274-282页

作者： Haojie Ma Zhenyu Guo Cong Gai Cuicui Cheng Jinkun Zhang Yuxin Zhang Luping Yang wandi feng Yushan Gao Hongmei Sun School of Chinese Medicine Beijing University of Chinese MedicineBeijing102488China

Objective:Buyinqianzheng Formula(BYQZF)is clinically employed in traditional Chinese medicine to treat Parkinson's disease(PD)by improving mitochondrial ***,the underlying mechanisms by which BYQZF affects mitochondrial morphology remain ***,we observed the effects of BYQZF on mitochondria from the perspective of the PINK1/Parkin ***:Cell survival rates were assessed by Cell Counting Kit-8 *** levels of PINK1 and Parkin mRNA were examined by *** expression levels of PINK1,PINK1-Ser228,Parkin,Parkin-Ser65,Drp1,and Drp1-Ser637 were examined by western ***1,Parkin,and MitoTracker?Red CMXRos(MTR)were stained by triple-labeled immunofluorescence,and observed under laser confocal ***:Cell survival rate,mitochondrial form factor,mean length and number of mitochondrial network branches,mitochondrial activity,m RNA expression levels of PINK1 and Parkin,and protein expression levels of PINK1,Parkin,and Drp1-Ser637 were reduced after 1-methyl-4-phenylpyridinium(MPP^(+))*** contrast,Pearson's correlation coefficients between PINK1 and Parkin,and between Parkin and MTR,as well as protein expression levels of PINK1-Ser228,Parkin-Ser65,and Drp1 increased significantly after MPP^(+) *** with BYQZF increased cell survival rate,mitochondrial form factor,mean length and number of mitochondrial network branches,mitochondrial activity,m RNA expression levels of PINK1 and Parkin,and expression of PINK1,Parkin,and Drp1-Ser637 ***'s correlation coefficients between PINK1 and Parkin,and between Parkin and MTR,as well as protein expression levels of PINK1-Ser228,Parkin-Ser65,and Drp1 decreased after BYQZF ***:These results demonstrate that BYQZF has a protective effect on mitochondrial molecular mechanisms in the PD cell model,and the mechanism is related to the PINK1/Parkin pathway.

关键词： BYQZF Parkinson's disease MPP^(+) Mitochondria PINK1/Parkin pathway

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Mechanism of Buyin Qianzheng Fang on preventing dopamine neuron from apoptosis by regulating intracellular Ca^(2+) in PD Mice

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解剖学杂志 2021年第S1期44卷 228-229页

作者： Zhao Haihong feng wandi Ma Haojie Cheng Cuicui Zhou Mengqi Gao Yushan Gai Cong Sun Hongsun Department of Anatomy Beijing University of Chinese MedicineBeijing 100029

The purpose of this study is to investigate the possible protective mechanism of Buyin Qianzheng Fang(BYQZF)on endoplasmic reticular and mitochondrial function through intracellular Ca^(2+) to protect dopamine neurons in Parkinson's disease mice model.C57BL/6 mice were randomly divided into normal group,model group,BYQZF *** behavior of mice was observed by climbing and beam hang tests.

关键词： C57BL/6 dopamine protective

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Mechanism of Buyin Qianzheng Fang on preventing dopamine neuron from apoptosis by regulating intracellular Ca2+ in PD Mice

Mechanism of Buyin Qianzheng Fang on preventing dopamine neu...

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中国解剖学会2021年年会

作者： Zhao Haihong feng wandi Ma Haojie Cheng Cuicui Zhou Mengqi Gao Yushan Gai Cong Sun Hongsun Department of Anatomy Beijing University of Chinese Medicine

The purpose of this study is to investigate the possible protective mechanism of Buyin Qianzheng Fang(BYQZF) on endoplasmic reticular and mitochondrial function through intracellular Ca to protect dopamine neurons in Parkinson’s disease mice model.C57BL/6 mice were randomly divided into normal group,model group, BYQZF group.

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Influences of Buyin Qianzheng Fang on mitochondria based on Drp1-Ser637 phosphorylation in PD mice

Influences of Buyin Qianzheng Fang on mitochondria based on ...

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中国解剖学会2019年年会

作者： Haihong Zhao Tianyao Qiang wandi feng Haojie Ma Yuan Chai Mengqi Zhou Yushan Gao Cong Gai Hongsun Sun Department of Anatomy Beijing University of Chinese Medicine

＜正＞The purpose of this study is to investigate the possible protective mechanism of Buyin Qianzheng Fang（BYQZF） on brain mitochondria through Drp1 and its phosphorylation site Ser637 in Parkinson’s disease （PD）mice model induced by MPTP.C57BL/6 mice were randomly divided into normal group,model group,Chinese medicine group,madopar *** behavior of mice was observed by climbing and gripping ***

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Effect of Timosaponin B-Ⅱ on morphology and function of mitochondria in PD cell model

Effect of Timosaponin B-Ⅱ on morphology and function of mit...

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中国解剖学会2021年年会

作者： Zhou Mengqi Gai Cong feng wandi Ma Haojie Cheng Cuicui Zhao Haihong Zhang Yuxin Zhang Jinkun Yang Luping Sun Hongmei Department of Anatomy College of Traditional Chinese MedicineBeijing University of Chinese Medicine

Explore the effect of Timosaponin B-Ⅱon morphology and function of mitochondria in Parkinson’s disease (PD) cell model,and lay the foundation for screening and-mechanism research of anti-Parkinson’s disease *** PD cell model was constructed by applying MPPto SH-SY5Y cells for 48 h, and they were treated with low,medium and high concentrations of Timosaponin B-Ⅱ.CCK-8 method was used to detect the survival rate of cells

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The construction of OPA1 overexpression plasmid and the cell model

The construction of OPA1 overexpression plasmid and the cell...

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中国解剖学会2021年年会

作者： Ma Haojie Gai Cong feng wandi Cheng Cuicui Zhou Mengqi Zhang Jinkun Zhang Yuxin Yang Luping Guo Zhenyu Sun Hongmei Department of Anatomy School of Chinese MedicineBeijing University of Chinese Medicine

The purpose of this study is to construct OPA1 overexpression plasmid and transfected into human neuroblastoma SH-SY5Y cells to test the overexpression *** neuroblastoma SH-SY5Y cells were transfected with the OPA1 overexpression plasmid by Lipo3000 transfection reagent in liposome transduction technology.A total of 3 groups were set up:the control group, negative controlgroup,and OPA1 overexpression model group.

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