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  1. Article: The Traditional Chinese Medicine Formula FTZ Protects against Cardiac Fibrosis by Suppressing the TGF

    Zhang, Yue / Wang, Dongwei / Wu, Kaili / Shao, Xiaoqi / Diao, Hongtao / Wang, Zhiying / Sun, Mengxian / Huang, Xueying / Li, Yun / Tang, Xinyuan / Yan, Meiling / Guo, Jiao

    Evidence-based complementary and alternative medicine : eCAM

    2022  Volume 2022, Page(s) 5642307

    Abstract: Background: Fu fang Zhen Zhu Tiao Zhi (FTZ) is a patented preparation of Chinese herbal medicine that has been used as a natural medicine to treat several chronic diseases including cardiovascular disease. However, its effects on cardiac fibrosis remain ...

    Abstract Background: Fu fang Zhen Zhu Tiao Zhi (FTZ) is a patented preparation of Chinese herbal medicine that has been used as a natural medicine to treat several chronic diseases including cardiovascular disease. However, its effects on cardiac fibrosis remain unclear. Therefore, this study was designed to investigate the effects and potential mechanisms of FTZ in treating cardiac fibrosis.
    Methods: FTZ was administered to mice by oral gavage daily at a dosage of 1.2 g/kg or 2.4 g/kg of body weight for 7 weeks after a transverse aorta constriction (TAC) surgery. Doppler echocardiography, hematoxylin and eosin staining, and Masson's trichrome staining were used to assess the effect of FTZ on the cardiac structure and function of mice that had undergone TAC. EdU and wound-healing assays were performed to measure the proliferative and migratory abilities of cardiac fibroblasts. Western blotting and qRT-PCR were used to determine the expression of TGF
    Results: FTZ treatment reduced collagen synthesis, attenuated cardiac fibrosis, and improved cardiac function in mice subjected to TAC. Moreover, FTZ treatment prevented the proliferation and migration of cardiac fibroblasts and reduced Ang-II-induced collagen synthesis. Furthermore, FTZ downregulated the expression of TGF
    Conclusion: FTZ alleviated the proliferation and migration of cardiac fibroblasts and suppressed collagen synthesis via the TGF
    Language English
    Publishing date 2022-04-19
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2171158-6
    ISSN 1741-4288 ; 1741-427X
    ISSN (online) 1741-4288
    ISSN 1741-427X
    DOI 10.1155/2022/5642307
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5995: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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  2. Article ; Online: MicroRNA-24-3p alleviates cardiac fibrosis by suppressing cardiac fibroblasts mitophagy via downregulating PHB2.

    Zhang, Yue / Wang, Zhiying / Lan, Dingming / Zhao, Jingjing / Wang, Lexun / Shao, Xiaoqi / Wang, Dongwei / Wu, Kaili / Sun, Mengxian / Huang, Xueying / Yan, Meiling / Liang, Haihai / Rong, Xianglu / Diao, Hongtao / Guo, Jiao

    Pharmacological research

    2022  Volume 177, Page(s) 106124

    Abstract: Cardiac fibrosis is a pathological process of multiple cardiovascular diseases, which may lead to heart failure. Studies have shown that microRNAs (miRNAs) play critical roles in regulating mitophagy and cardiac fibrosis. We found that miR-24-3p ... ...

    Abstract Cardiac fibrosis is a pathological process of multiple cardiovascular diseases, which may lead to heart failure. Studies have shown that microRNAs (miRNAs) play critical roles in regulating mitophagy and cardiac fibrosis. We found that miR-24-3p expression was significantly downregulated in transverse aortic constriction (TAC) mice and cardiac fibroblasts (CFs) treated with Ang Ⅱ. We also found that, apart from improving cardiac structure and function, forced expression of miR-24-3p not only reduced the levels of collagen and α-SMA but also inhibited proliferation and migration of CFs. Next, our research proved that miR-24-3p suppressed the progression of mitophagy, autophagic flux, and the levels of mitophagy-related proteins in cardiac fibrosis models. Further analysis showed that PHB2 was a direct target of miR-24-3p. Finally, experiments showed that the knockdown of PHB2 reversed Ang Ⅱ-induced fibrosis in CFs. The results of our study suggests that increased expression of miR-24-3p contributes to the reduction of cardiac fibrosis and that it might be targeted therapeutically to alleviate cardiac fibrosis.
    MeSH term(s) Animals ; Cells, Cultured ; Fibroblasts/metabolism ; Fibrosis ; Mice ; Mice, Inbred C57BL ; MicroRNAs/metabolism ; Mitophagy ; Myocardium/metabolism ; Prohibitins/metabolism
    Chemical Substances MicroRNAs ; Mirn24 microRNA, mouse ; Phb2 protein, mouse ; Prohibitins
    Language English
    Publishing date 2022-02-09
    Publishing country Netherlands
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1003347-6
    ISSN 1096-1186 ; 0031-6989 ; 1043-6618
    ISSN (online) 1096-1186
    ISSN 0031-6989 ; 1043-6618
    DOI 10.1016/j.phrs.2022.106124
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 721: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  3. Article ; Online: FTZ protects against cardiac hypertrophy and oxidative injury via microRNA-214 / SIRT3 signaling pathway.

    Zhang, Yue / Sun, Mengxian / Wang, Dongwei / Hu, Yaju / Wang, Ruonan / Diao, Hongtao / Shao, Xiaoqi / Li, Yun / Li, Xu / Leng, Mingyang / Wang, Lexun / Yan, Meiling / Rong, Xianglu / Guo, Jiao

    Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie

    2022  Volume 148, Page(s) 112696

    Abstract: Background: Despite the fact that the initial hypertrophic response to ventricular pressure overload is thought to be compensatory, prolonged stress often leads to heart failure. Previous studies have shown that the Fufang-Zhenzhu-Tiaozhi (FTZ) formula ... ...

    Abstract Background: Despite the fact that the initial hypertrophic response to ventricular pressure overload is thought to be compensatory, prolonged stress often leads to heart failure. Previous studies have shown that the Fufang-Zhenzhu-Tiaozhi (FTZ) formula is beneficial for the treatment of dyslipidemia and hyperglycemia. However, the effects of FTZ on cardiac hypertrophy remain unclear.
    Objective: The aim of this study is to evaluate the protective effects of FTZ on cardiac hypertrophy and determine the underlying mechanisms.
    Methods: TAC was utilized to establish a cardiac hypertrophy animal model, and FTZ was given via gavage for four weeks. Next, echocardiographic measurements were made. The morphology of mouse cardiomyocytes was examined using H&E and WGA staining. In vitro, the neonatal cardiomyocytes were stimulated with angiotensin Ⅱ (Ang Ⅱ). In addition to measuring the size of cardiomyocytes, qRT-PCR and western blotting were conducted to measure cardiac stress markers and pathway.
    Results: According to our findings, FTZ alleviated cardiac hypertrophy in mice and cell models. Furthermore, expression of miR-214 was down-regulated following FTZ, whereas the effect of FTZ therapy was reversed using miR-214 transfection. Furthermore, the expression of Sirtuin 3 (SIRT3) was decreased in Ang Ⅱ-induced oxidative damage, which was associated with a reduction in SOD-1, GPX1, and HO-1 and an increase in MDA, while SIRT3 expression was restored following FTZ treatment.
    Conclusions: Collectively, these findings indicate that FTZ is a protective factor for cardiac hypertrophy due to its regulation of the miR-214-SIRT3 axis, which suggests that FTZ may be a therapeutic target for cardiac hypertrophy.
    MeSH term(s) Angiotensin II/metabolism ; Animals ; Cardiomegaly/drug therapy ; Drugs, Chinese Herbal ; Mice ; Mice, Inbred C57BL ; MicroRNAs/metabolism ; Myocytes, Cardiac ; Oxidative Stress ; Signal Transduction ; Sirtuin 3/genetics ; Sirtuin 3/metabolism
    Chemical Substances Drugs, Chinese Herbal ; MicroRNAs ; Mirn214 microRNA, mouse ; Sirt3 protein, mouse ; fufang-zhenzhu-tiaozhi ; Angiotensin II (11128-99-7) ; Sirtuin 3 (EC 3.5.1.-)
    Language English
    Publishing date 2022-02-16
    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.2022.112696
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Ud II Zs.198: Show issues Location:
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    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

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  4. Article: Fu Fang Zhen Zhu Tiao Zhi Capsules Protect against Myocardial Ischemia by Inhibiting Cardiomyocyte Pyroptosis.

    Shao, Xiaoqi / Huang, Bingying / Tan, Huiling / Wang, Ruonan / Huang, Xueying / Diao, Hongtao / Cheng, Jiawen / Sun, Mengxian / Wang, Dongwei / Wu, Kaili / Yan, Meiling / Rong, Xianglu / Zhang, Yue / Guo, Jiao

    Evidence-based complementary and alternative medicine : eCAM

    2022  Volume 2022, Page(s) 4752360

    Abstract: Background: Fu Fang Zhen Zhu Tiao Zhi (FTZ) is a traditional Chinese herbal prescription widely used to treat dyslipidemia, metabolic diseases, and diabetic coronary disorders. Cardiomyocyte death and loss of regenerative ability cause cardiac ... ...

    Abstract Background: Fu Fang Zhen Zhu Tiao Zhi (FTZ) is a traditional Chinese herbal prescription widely used to treat dyslipidemia, metabolic diseases, and diabetic coronary disorders. Cardiomyocyte death and loss of regenerative ability cause cardiac dysfunction and heart failure. FTZ can effectively treat diabetic cardiomyopathy and macrovascular diseases; however, the mechanism behind the phenomenon is still unclear. Here, we determined the mechanism of action of FTZ in treating myocardial infarction.
    Methods: Male C57BL/6 mice were treated with 2.4 or 1.2 g/kg FTZ, or administered saline by oral gavage daily for four weeks, and a 24-hour ligation was administered to the artery. Echocardiography was used to evaluate cardiac function. Hematoxylin and eosin and Evans blue/triphenyltetrazolium chloride staining were carried out by staining the cardiac tissue, used to evaluate cardiac function and infarct size. Using western blotting and reverse transcriptase-polymerase chain reaction, we determined the relative levels of NOD-like receptor protein (NLRP) 3, ASC, cleaved caspase-l (C-Caspase-1), GSDMD, and GSDMD-N. TUNEL, immunohistochemical, and immunofluorescence staining were used to determine cell death and NLRP3 expression. An enzyme-linked immunosorbent assay (ELISA) was used to detect the levels of interleukin (IL)-1
    Results: FTZ reduced ischemia-induced cardiomyocyte cell death
    Conclusion: FTZ could preserve cardiac function resulting from ischemic insult by inhibiting pyroptosis, which was partially reversed by NLRP3 overexpression, indicating that NLRP3 could be a potential target of FTZ in treating myocardial infarction.
    Language English
    Publishing date 2022-11-02
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2171158-6
    ISSN 1741-4288 ; 1741-427X
    ISSN (online) 1741-4288
    ISSN 1741-427X
    DOI 10.1155/2022/4752360
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5995: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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    ab Jg. 2022: Lesesaal (EG)

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  5. Article ; Online: Identifying a transport mechanism of dust aerosols over South Asia to the Tibetan Plateau: A case study.

    Wang, Tianhe / Tang, Jingyi / Sun, Mengxian / Liu, Xinwei / Huang, Yuxia / Huang, Jianping / Han, Ying / Cheng, Yifan / Huang, Zhongwei / Li, Jiming

    The Science of the total environment

    2020  Volume 758, Page(s) 143714

    Abstract: Dust aerosol, one of the important light-absorbing impurities in snow and ice sheets in the Tibet Plateau (TP), can significantly affect the magnitude and timing of snow melting and glacier recession by altering the surface albedo. It is thus of great ... ...

    Abstract Dust aerosol, one of the important light-absorbing impurities in snow and ice sheets in the Tibet Plateau (TP), can significantly affect the magnitude and timing of snow melting and glacier recession by altering the surface albedo. It is thus of great importance to understand the potential source and transport mechanism of the dust aerosol over the TP. A typical dust storm case, erupted from the Thar Desert (ThD) in South Asia on 1 to 4 May 2018, was selected to understand synoptic causes and a transport mechanism to the TP using the latest Second Modern-Era Retrospective analysis for Research and Applications (MERRA-2) reanalysis data. Comparing with active/passive satellite-based and AERONET-based observations, the MERRA-2 data provide both the spatio-temporal distribution and evolution process of the dust aerosol more accurately. This study also found that the entire Indian-Gangetic Plain (IGP), Southern India, the Bay of Bengal, and even the TP were influenced by the dust event. The synoptic analysis showed that the dust storm was caused jointly by an upper-level jet stream (ULJS), an upper trough and the subtropical high. A typical south-north secondary circulation adjacent its exit zone, mainly triggered by the ULJS, promoted much stronger and higher vertical uplift of the dust aerosols over the ThD. Consequently, those uplifted dust particles were easily transported to the TP across the majestic Himalayas by the southerly airflows in front of the low-pressure trough over Afghanistan and the southern branch trough over the Bengal Bay. These results indicate that dust aerosol and anthropogenic pollutions constrained and driven by the typical atmospheric circulation condition from South Asia are likely to be transported to the TP. Therefore, it is necessary to further pay attention to the influence of dust aerosols from South Asia on the weather and climate in the TP and its downstream areas.
    Language English
    Publishing date 2020-11-14
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 121506-1
    ISSN 1879-1026 ; 0048-9697
    ISSN (online) 1879-1026
    ISSN 0048-9697
    DOI 10.1016/j.scitotenv.2020.143714
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 949: Show issues Location:
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