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  1. Article: Kai Xin San

    Xu, Yu-Min / Wang, Xin-Chen / Xu, Ting-Ting / Li, Hong-Ying / Hei, Shang-Yan / Luo, Na-Chuan / Wang, Hong / Zhao, Wei / Fang, Shu-Huan / Chen, Yun-Bo / Guan, Li / Fang, Yong-Qi / Zhang, Shi-Jie / Wang, Qi / Liang, Wei-Xiong

    Neural regeneration research

    2019  Volume 14, Issue 5, Page(s) 794–804

    Abstract: Kai Xin San (KXS, containing ginseng, hoelen, polygala, and acorus), a traditional Chinese herbal ...

    Abstract Kai Xin San (KXS, containing ginseng, hoelen, polygala, and acorus), a traditional Chinese herbal compound, has been found to regulate cognitive dysfunction; however, its mechanism of action is still unclear. In this study, 72 specific-pathogen-free male Kunming mice aged 8 weeks were randomly divided into a vehicle control group, scopolamine group, low-dose KXS group, moderate-dose KXS group, high-dose KXS group, and positive control group. Except for the vehicle control group and scopolamine groups (which received physiological saline), the doses of KXS (0.7, 1.4 and 2.8 g/kg per day) and donepezil (3 mg/kg per day) were gastrointestinally administered once daily for 2 weeks. On day 8 after intragastric treatment, the behavioral tests were carried out. Scopolamine group and intervention groups received scopolamine 3 mg/kg per day through intraperitoneal injection. The effects of KXS on spatial learning and memory, pathological changes of brain tissue, expression of apoptosis factors, oxidative stress injury factors, synapse-associated protein, and cholinergic neurotransmitter were measured. The results confirmed the following. (1) KXS shortened the escape latency and increased residence time in the target quadrant and the number of platform crossings in the Morris water maze. (2) KXS increased the percentage of alternations between the labyrinth arms in the mice of KXS groups in the Y-maze. (3) Nissl and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling staining revealed that KXS promoted the production of Nissl bodies and inhibited the formation of apoptotic bodies. (4) Western blot assay showed that KXS up-regulated the expression of anti-apoptotic protein Bcl-2 and inhibited the expression of pro-apoptotic protein Bax. KXS up-regulated the expression of postsynaptic density 95, synaptophysin, and brain-derived neurotrophic factor in the cerebral cortex and hippocampus. (5) KXS increased the level and activity of choline acetyltransferase, acetylcholine, superoxide dismutase, and glutathione peroxidase, and reduced the level and activity of acetyl cholinesterase, reactive oxygen species, and malondialdehyde through acting on the cholinergic system and reducing oxidative stress damage. These results indicate that KXS plays a neuroprotective role and improves cognitive function through reducing apoptosis and oxidative stress, and regulating synapse-associated protein and cholinergic neurotransmitters.
    Language English
    Publishing date 2019-01-28
    Publishing country India
    Document type Journal Article
    ZDB-ID 2388460-5
    ISSN 1876-7958 ; 1673-5374
    ISSN (online) 1876-7958
    ISSN 1673-5374
    DOI 10.4103/1673-5374.249227
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: The Chinese medicine Xin-tong-tai granule protects atherosclerosis by regulating oxidative stress through NOX/ROS/NF-κB signal pathway.

    Wei, Jia-Ming / Yuan, Hui / Liu, Cheng-Xin / Wang, Zi-Yan / Shi, Min / Guo, Zhi-Hua / Li, Ya

    Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie

    2023  Volume 165, Page(s) 115200

    Abstract: Background: Xin-tong-tai Granule (XTTG), a traditional Chinese medicine, has been used to treat ...

    Abstract Background: Xin-tong-tai Granule (XTTG), a traditional Chinese medicine, has been used to treat atherosclerosis (AS), but its mechanism is poorly understood. Intriguingly, oxidative stress has been recognized as vital factors in the treatment of atherosclerosis.
    Purpose: This study aims to explore the potential mechanism of XTTG for treating AS.
    Methods: An in-vivo model of AS was established by feeding ApoE
    Results: XTTG improved blood lipid levels and pathological aortic changes of ApoE
    Conclusion: XTTG can inhibit NOX/ROS/NF-κB signaling pathway, reduce damages caused by oxidative stress, and exert anti-AS effects.
    MeSH term(s) Animals ; Humans ; Mice ; Apolipoproteins E/genetics ; Apolipoproteins E/metabolism ; Atherosclerosis/drug therapy ; Atherosclerosis/prevention & control ; Atherosclerosis/genetics ; Lipoproteins, LDL/pharmacology ; NF-kappa B/metabolism ; Oxidative Stress ; Reactive Oxygen Species/metabolism ; Signal Transduction ; Superoxide Dismutase/metabolism ; Drugs, Chinese Herbal/pharmacology
    Chemical Substances Apolipoproteins E ; Lipoproteins, LDL ; NF-kappa B ; Reactive Oxygen Species ; Superoxide Dismutase (EC 1.15.1.1) ; Drugs, Chinese Herbal
    Language English
    Publishing date 2023-07-26
    Publishing country France
    Document type Journal Article
    ZDB-ID 392415-4
    ISSN 1950-6007 ; 0753-3322 ; 0300-0893
    ISSN (online) 1950-6007
    ISSN 0753-3322 ; 0300-0893
    DOI 10.1016/j.biopha.2023.115200
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Mechanisms of Lian-Gui-Ning-Xin-Tang in the treatment of arrhythmia: Integrated pharmacology and in vivo pharmacological assessment.

    Chen, Jinhong / Liu, Zhichao / Deng, Fangjun / Liang, Jiayu / Fan, Boya / Zhen, Xin / Tao, Rui / Sun, Lili / Zhang, Shaoqiang / Cong, Zidong / Li, Xiaofeng / Du, Wuxun

    Phytomedicine : international journal of phytotherapy and phytopharmacology

    2022  Volume 99, Page(s) 153989

    Abstract: Background: Lian-Gui-Ning-Xin-Tang (LGNXT), a classical traditional Chinese medicine (TCM) formula ...

    Abstract Background: Lian-Gui-Ning-Xin-Tang (LGNXT), a classical traditional Chinese medicine (TCM) formula, has been widely used in clinical practice and has shown satisfactory efficacy in the treatment of arrhythmias. However, its mechanism of action in the treatment of arrhythmias is still unknown. Moreover, the complex chemical composition and therapeutic targets of LGNXT pose a challenge in pharmacological research.
    Purpose: To analyze the active compounds and action mechanisms of LGNXT for the treatment of arrhythmias.
    Methods: Here, we used an integrated pharmacology approach to identify the potential active compounds and mechanisms of action of LGNXT in treating arrhythmias. Potential active compounds in LGNXT were identified using ultra-performance liquid chromatography-quadrupole-time-of-flight mass spectrometry (UPLC-Q-TOF/MS) and the potential related targets of these compounds were predicted using an integrated in silico approach. The obtained targets were mapped onto relevant databases to identify their corresponding pathways, following the experiments that were conducted to confirm whether the presumptive results of systemic pharmacology were correct.
    Results: Eighty-three components were identified in herbal materials and in animal plasma using UPLC-Q-TOF/MS and were considered the potential active components of LGNXT. Thirty key targets and 57 Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways were identified as possible targets and pathways involved in LGNXT-mediated treatment using network pharmacology, with the cyclic adenosine monophosphate (cAMP)/protein kinase A (PKA)/Ca
    Conclusions: The findings of this study revealed that preventing intracellular Ca
    Language English
    Publishing date 2022-02-12
    Publishing country Germany
    Document type Journal Article
    ZDB-ID 1205240-1
    ISSN 1618-095X ; 0944-7113
    ISSN (online) 1618-095X
    ISSN 0944-7113
    DOI 10.1016/j.phymed.2022.153989
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article: Cardiac Overexpression of XIN Prevents Dilated Cardiomyopathy Caused by

    Li, Bin / Guo, Yifan / Zhan, Yongkun / Zhou, Xinyan / Li, Yongbo / Zhao, Chao / Sun, Ning / Xu, Chen / Liang, Qianqian

    Frontiers in cell and developmental biology

    2021  Volume 9, Page(s) 691749

    Abstract: ... ...

    Abstract TNNT2
    Language English
    Publishing date 2021-06-17
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2737824-X
    ISSN 2296-634X
    ISSN 2296-634X
    DOI 10.3389/fcell.2021.691749
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Bu-Shen-Ning-Xin decoction inhibits macrophage activation to ameliorate premature ovarian insufficiency-related osteoimmune disorder via FSH/FSHR pathway.

    Sun, Hongmei / Qi, Qing / Pan, Xinyao / Zhou, Jing / Wang, Jing / Li, Lisha / Li, Dajing / Wang, Ling

    Drug discoveries & therapeutics

    2024  

    Abstract: ... osteoimmune disorder currently. Bu-Shen-Ning-Xin decoction (BSNXD) displayed a favorable role in treating ...

    Abstract Limited studies are associated with premature ovarian insufficiency (POI)-related osteoimmune disorder currently. Bu-Shen-Ning-Xin decoction (BSNXD) displayed a favorable role in treating postmenopausal osteoporosis. However, its impact on the POI-related osteoimmune disorder remains unclear. The study primarily utilized animal experiments and network pharmacology to investigate the effects and underlying mechanisms of BSNXD on the POI-related osteoimmune disorder. First, a 4-vinylcyclohexene dioxide (VCD)-induced POI murine model was conducted to explore the therapeutical action of BSNXD. Second, we analyzed the active compounds of BSNXD and predicted their potential mechanisms for POI-related osteoimmune disorder via network pharmacology, further confirmed by molecular biology experiments. The results demonstrated that VCD exposure led to elevated follicle-stimulating hormone (FSH) levels, a 50% reduction in the primordial follicles, bone microstructure changes, and macrophage activation, indicating an osteoimmune disorder. BSNXD inhibited macrophage activation and osteoclast differentiation but did not affect serum FSH and estradiol levels in the VCD-induced POI model. Network pharmacology predicted the potential mechanisms of BSNXD against the POI-related osteoimmune disorder involving tumor necrosis factor α and MAPK signaling pathways, highlighting BSNXD regulated inflammation, hormone, and osteoclast differentiation. Further experiments identified BSNXD treatment suppressed macrophage activation via downregulating FSH receptor (FSHR) expression and inhibiting the phosphorylation of ERK and CCAAT enhancer binding proteins β. In conclusion, BSNXD regulated POI-related osteoimmune disorder by suppressing the FSH/FSHR pathway to reduce macrophage activation and further inhibiting osteoclastogenesis.
    Language English
    Publishing date 2024-04-17
    Publishing country Japan
    Document type Journal Article
    ZDB-ID 2568828-5
    ISSN 1881-784X ; 1881-784X
    ISSN (online) 1881-784X
    ISSN 1881-784X
    DOI 10.5582/ddt.2024.01006
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Kai-Xin-San ameliorates Alzheimer's disease-related neuropathology and cognitive impairment in APP/PS1 mice via the mitochondrial autophagy-NLRP3 inflammasome pathway.

    Shan, Xiaoxiao / Tao, Wenwen / Li, Junying / Tao, Wenkang / Li, Dawei / Zhou, Lele / Yang, Xuan / Dong, Chong / Huang, Shunwang / Chu, Xiaoqin / Zhang, Caiyun

    Journal of ethnopharmacology

    2024  Volume 329, Page(s) 118145

    Abstract: Ethnopharmacological relevance: Kai-Xin-San (KXS) is a classic famous prescription that has been ...

    Abstract Ethnopharmacological relevance: Kai-Xin-San (KXS) is a classic famous prescription that has been utilized for centuries to address dementia. New investigations have shown that the anti-dementia effect of KXS is connected with improved neuroinflammation. Nevertheless, the underlying mechanism is not well elucidated.
    Aim of the study: We propose to discover the ameliorative impact of KXS on Alzheimer's disease (AD) and its regulatory role on the mitochondrial autophagy-nod-like receptor protein 3 (NLRP3) inflammasome pathway.
    Materials and methods: The Y maze, Morris water maze, and new objection recognition tests were applied to ascertain the spatial learning and memory capacities of amyloid precursor protein/presenilin 1 (APP/PS1) mice after KXS-treatment. Meanwhile, the biochemical indexes of the hippocampus were detected by reagent kits. The pathological alterations and mitochondrial autophagy in the mice' hippocampus were detected utilizing hematoxylin and eosin (H&E), immunohistochemistry, immunofluorescence staining, and transmission electron microscopy. Besides, the PTEN-induced putative kinase 1 (PINK1)/Parkin and NLRP3 inflammasome pathways protein expressions were determined employing the immunoblot analysis.
    Results: The results of behavioral tests showed that KXS significantly enhanced the AD mice' spatial learning and memory capacities. Furthermore, KXS reversed the biochemical index levels and reduced amyloid-β protein deposition in AD mice brains. Besides, H&E staining showed that KXS remarkably ameliorated the neuronal damage in AD mice. Concurrently, the results of transmission electron microscopy suggest that KXS ameliorated the mitochondrial damage in microglia and promoted mitochondrial autophagy. Moreover, the immunofluorescence outcomes exhibited that KXS promoted the expression of protein 1 light chain 3B (LC3B) associated with microtubule and the generation of autophagic flux. Notably, the immunofluorescence co-localization results confirmed the presence of mitochondrial autophagy in microglia. Finally, KXS promoted the protein expressions of the PINK1/Parkin pathway and reduced the activation of NLRP3 inflammasome. Most importantly, these beneficial effects of KXS were attenuated by the mitochondrial autophagy inhibitor chloroquine.
    Conclusion: KXS ameliorates AD-related neuropathology and cognitive impairment in APP/PS1 mice by enhancing the mitochondrial autophagy and suppressing the NLRP3 inflammasome pathway.
    Language English
    Publishing date 2024-04-04
    Publishing country Ireland
    Document type Journal Article
    ZDB-ID 134511-4
    ISSN 1872-7573 ; 0378-8741
    ISSN (online) 1872-7573
    ISSN 0378-8741
    DOI 10.1016/j.jep.2024.118145
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  7. Article ; Online: Chinese medicinal formula Fu Xin decoction against chronic heart failure by inhibiting the NLRP3/caspase-1/GSDMD pyroptotic pathway.

    Zhang, Lei / Li, Yan / Fan, Cun-Dong / Jiang, Yong-Hao / Sheng, Li-Song / Song, Xu-Yu / Lin, Yu-Xing / Xue, Yi-Tao / Sun, Rong

    Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie

    2024  Volume 174, Page(s) 116548

    Abstract: ... NLRP3) inflammasome. Fu Xin decoction (FXD) is commonly used in clinical practice to treat CHF and ...

    Abstract Background: Various heart diseases ultimately lead to chronic heart failure (CHF). In CHF, the inflammatory response is associated with pyroptosis, which is mediated by the NOD-like receptor protein 3 (NLRP3) inflammasome. Fu Xin decoction (FXD) is commonly used in clinical practice to treat CHF and improve inflammatory conditions. However, the specific pharmacological mechanisms of action for FXD in these processes have yet to be fully understood.
    Purpose: The objective of this study was to examine the protective mechanism of FXT against CHF, both in H9c2 cells and mice.
    Method: A CHF mouse model was established, and the effect of FXD was observed via gavage. Cardiac function was evaluated using echocardiography, while serum BNP and LDH levels were analyzed to assess the severity of CHF. Hematoxylin and eosin staining (H&E) and Masson staining were performed to evaluate myocardial pathological changes, and TdT-mediated dUTP Nick-End Labeling staining was used to detect DNA damage. Additionally, doxorubicin was utilized to induce myocardial cell injury in H9c2 cells, establishing a relevant model. CCK8 was used to observe cell viability and detect LDH levels in the cell supernatant. Subsequently, the expression of pyroptosis-related proteins was detected using immunohistochemistry, immunofluorescence, and western blotting. Finally, the pharmacological mechanism of FXD against CHF was further validated by treating H9c2 cells with an NLRP3 activator and inducing NLRP3 overexpression.
    Result: According to current research findings, echocardiography demonstrated a significant improvement of cardiac function by FXD, accompanied by reduced levels of BNP and LDH, indicating the amelioration of cardiac injury in CHF mice. FXD exhibited the ability to diminish serum CRP and MCP inflammatory markers in CHF mice. The results of HE and Masson staining analyses revealed a significant reduction in pathological damage of the heart tissue following FXD treatment. The CCK8 assay demonstrated the ability of FXD to enhance H9c2 cell viability, improve cell morphology, decrease LDH levels in the cell supernatant, and alleviate cell damage. Immunohistochemistry, Western blotting, and immunofluorescence staining substantiated the inhibitory effect of FXD on the NLRP3/caspase-1/GSDMD pyroptosis signaling pathway in both CHF and H9c2 cell injury models. Ultimately, the administration of the NLRP3 activator (Nigericin) and the overexpression of NLRP3 counteract the effects of FXD on cardiac protection and pyroptosis inhibition in vitro.
    Conclusion: FXD exhibits a cardioprotective effect, improving CHF and alleviating pyroptosis by inhibiting the NLRP3/caspase-1/GSDMD pathway.
    Language English
    Publishing date 2024-04-09
    Publishing country France
    Document type Journal Article
    ZDB-ID 392415-4
    ISSN 1950-6007 ; 0753-3322 ; 0300-0893
    ISSN (online) 1950-6007
    ISSN 0753-3322 ; 0300-0893
    DOI 10.1016/j.biopha.2024.116548
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article: Research on the quality markers of antioxidant activity of Kai-Xin-San based on the spectrum-effect relationship.

    Shan, Xiaoxiao / Yang, Xuan / Li, Dawei / Zhou, Lele / Qin, Shaogang / Li, Junying / Tao, Wenkang / Peng, Can / Wei, Jinming / Chu, Xiaoqin / Wang, Haixuan / Zhang, Caiyun

    Frontiers in pharmacology

    2023  Volume 14, Page(s) 1270836

    Abstract: Background: ...

    Abstract Background:
    Language English
    Publishing date 2023-12-27
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2587355-6
    ISSN 1663-9812
    ISSN 1663-9812
    DOI 10.3389/fphar.2023.1270836
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article: Corrigendum: Systems pharmacology approach to investigate the mechanism of Kai-Xin-San in Alzheimer's disease.

    Luo, Yunxia / Li, Dongli / Liao, Yanfang / Cai, Chuipu / Wu, Qihui / Ke, Hanzhong / Liu, Xinning / Li, Huilin / Hong, Honghai / Xu, Yumin / Wang, Qi / Fang, Jiansong / Fang, Shuhuan

    Frontiers in pharmacology

    2023  Volume 14, Page(s) 1239060

    Abstract: This corrects the article DOI: 10.3389/fphar.2020.00381.]. ...

    Abstract [This corrects the article DOI: 10.3389/fphar.2020.00381.].
    Language English
    Publishing date 2023-10-06
    Publishing country Switzerland
    Document type Published Erratum
    ZDB-ID 2587355-6
    ISSN 1663-9812
    ISSN 1663-9812
    DOI 10.3389/fphar.2023.1239060
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  10. Article ; Online: Classic Famous Prescription Kai-Xin-San Ameliorates Alzheimer's Disease via the Wnt/β-Catenin Signaling Pathway.

    Shan, Xiaoxiao / Lv, Shujie / Huang, Peng / Zhang, Wei / Jin, Chuanshan / Liu, Yuanxu / Li, Yangyang / Jia, Yong / Chu, Xiaoqin / Peng, Can / Zhang, Caiyun

    Molecular neurobiology

    2023  Volume 61, Issue 4, Page(s) 2297–2312

    Abstract: Kai-Xin-San (KXS) is a classic famous prescription composed of Polygalae Radix, Ginseng Radix et ...

    Abstract Kai-Xin-San (KXS) is a classic famous prescription composed of Polygalae Radix, Ginseng Radix et Rhizoma, Acori Tatarinowii Rhizoma, and Poria. Clinically, KXS is effective in treating amnesia and regulating cognitive dysfunction of Alzheimer's disease (AD), whereas its mechanism of action is still unclear. In this study, the AD model rats were established by combining intraperitoneal injection of D-galactose (150 mg/kg/day) and intracerebral injection of Aβ
    MeSH term(s) Rats ; Animals ; Alzheimer Disease/metabolism ; Caspase 3/metabolism ; Glycogen Synthase Kinase 3 beta/metabolism ; beta Catenin/metabolism ; Wnt Signaling Pathway ; bcl-2-Associated X Protein ; Disease Models, Animal ; Drugs, Chinese Herbal
    Chemical Substances Kai-Xin-San ; Caspase 3 (EC 3.4.22.-) ; Glycogen Synthase Kinase 3 beta (EC 2.7.11.1) ; beta Catenin ; bcl-2-Associated X Protein ; Drugs, Chinese Herbal
    Language English
    Publishing date 2023-10-24
    Publishing country United States
    Document type Journal Article
    ZDB-ID 645020-9
    ISSN 1559-1182 ; 0893-7648
    ISSN (online) 1559-1182
    ISSN 0893-7648
    DOI 10.1007/s12035-023-03707-y
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