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  1. Article ; Online: Exploring the Potential Mechanism of Tang-Shen-Ning Decoction against Diabetic Nephropathy Based on the Combination of Network Pharmacology and Experimental Validation

    Jiajun Liang / Jiaxin He / Yanbin Gao / Zhiyao Zhu

    Evidence-Based Complementary and Alternative Medicine, Vol

    2021  Volume 2021

    Abstract: Background. Diabetic nephropathy (DN) has become one of the leading causes of the end-stage renal disease (ESRD). Tang-Shen-Ning (TSN) decoction, an effective Traditional Chinese formula for DN, can improve the renal function and inhibit renal fibrosis ... ...

    Abstract Background. Diabetic nephropathy (DN) has become one of the leading causes of the end-stage renal disease (ESRD). Tang-Shen-Ning (TSN) decoction, an effective Traditional Chinese formula for DN, can improve the renal function and inhibit renal fibrosis in DN. However, its potential mechanism is still unexplored. Methods. A network pharmacology approach was employed in this study, including screening for differential expressed genes of DN (DN-DEGs), protein-protein interaction (PPI) network analysis, and GO and KEGG enrichment analysis. Besides, a rat model was established to verify the potential effect of TSN in DN. Results. Twenty-three TSN-related DN-DEGs targets were identified. These genes were associated with decreased glomerular filtration rate (GFR) DN. The enrichment analysis suggested that the inhibition of renal fibrosis and inflammation through growth factors and chemokines is the potential mechanism through which TSN improves DN. TSN reduced renal fibrosis and improved pathological damage in the kidney in vivo through the regulation of GJA1, CTGF, MMP7, and CCL5, which are genes associated with ECM deposition. Conclusion. This study revealed that TSN improves DN through a multicomponent, multitarget, and multipathway synergy. We provide a scientific basis for potential targets for TSN use to treat DN, yet further experimental validation is needed to investigate these targets and mechanisms.
    Keywords Other systems of medicine ; RZ201-999
    Language English
    Publishing date 2021-01-01T00:00:00Z
    Publisher Hindawi Limited
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  2. Article ; Online: Effect of Tongxinluo on Podocyte Apoptosis via Inhibition of Oxidative Stress and P38 Pathway in Diabetic Rats

    Fangqiang Cui / Yanbin Gao / Wenjing Zhao / Dawei Zou / Zhiyao Zhu / Xiaoming Wu / Nianxiu Tian / Xiaolei Wang / Jing Liu / Yu Tong

    Evidence-Based Complementary and Alternative Medicine, Vol

    2016  Volume 2016

    Abstract: Diabetic nephropathy (DN) has been the leading cause of end-stage renal disease (ESRD). Podocyte apoptosis is a main mechanism of progression of DN. It has been demonstrated that activated P38 and caspase-3 induced by oxidative stress mainly account for ... ...

    Abstract Diabetic nephropathy (DN) has been the leading cause of end-stage renal disease (ESRD). Podocyte apoptosis is a main mechanism of progression of DN. It has been demonstrated that activated P38 and caspase-3 induced by oxidative stress mainly account for increased podocyte apoptosis and proteinuria in DN. Meanwhile, Tongxinluo (TXL) can ameliorate renal structure disruption and dysfunction in DN patients in our clinical practice. However, the effect of TXL on podocyte apoptosis and P38 pathway remains unclear. To explore the effect of TXL on podocyte apoptosis and its molecular mechanism in DN, our in vivo and in vitro studies were performed. TXL attenuated oxidative stress in podocyte in DN in our in vivo and in vitro studies. Moreover, TXL inhibited the activation of P38 and caspase-3. Bcl-2 and Bax expression was partially restored by TXL treatment in our in vivo and in vitro studies. More importantly, TXL decreased podocyte apoptosis in diabetic rats and high glucose cultured podocyte. In conclusion, TXL protects podocyte from apoptosis in DN, partially through its antioxidant effect and inhibiting of the activation of P38 and caspase-3.
    Keywords Other systems of medicine ; RZ201-999
    Subject code 610
    Language English
    Publishing date 2016-01-01T00:00:00Z
    Publisher Hindawi Limited
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  3. Article ; Online: Effects of Chinese Medicine Tong xinluo on Diabetic Nephropathy via Inhibiting TGF-β1-Induced Epithelial-to-Mesenchymal Transition

    Na Zhang / Yanbin Gao / Dawei Zou / Jinyang Wang / Jiaoyang Li / Shengnan Zhou / Zhiyao Zhu / Xuan Zhao / Liping Xu / Haiyan Zhang

    Evidence-Based Complementary and Alternative Medicine, Vol

    2014  Volume 2014

    Keywords Medicine (General) ; R5-920 ; Medicine ; R
    Language English
    Publishing date 2014-01-01T00:00:00Z
    Publisher Hindawi Publishing Corporation
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  4. Article ; Online: Effects of Chinese Medicine Tong xinluo on Diabetic Nephropathy via Inhibiting TGF-β1-Induced Epithelial-to-Mesenchymal Transition

    Na Zhang / Yanbin Gao / Dawei Zou / Jinyang Wang / Jiaoyang Li / Shengnan Zhou / Zhiyao Zhu / Xuan Zhao / Liping Xu / Haiyan Zhang

    Evidence-Based Complementary and Alternative Medicine, Vol

    2014  Volume 2014

    Abstract: Diabetic nephropathy (DN) is a major cause of chronic kidney failure and characterized by interstitial and glomeruli fibrosis. Epithelial-to-mesenchymal transition (EMT) plays an important role in the pathogenesis of DN. Tong xinluo (TXL), a Chinese ... ...

    Abstract Diabetic nephropathy (DN) is a major cause of chronic kidney failure and characterized by interstitial and glomeruli fibrosis. Epithelial-to-mesenchymal transition (EMT) plays an important role in the pathogenesis of DN. Tong xinluo (TXL), a Chinese herbal compound, has been used in China with established therapeutic efficacy in patients with DN. To investigate the molecular mechanism of TXL improving DN, KK-Ay mice were selected as models for the evaluation of pathogenesis and treatment in DN. In vitro, TGF-β1 was used to induce EMT. Western blot (WB), immunofluorescence staining, and real-time polymerase chain reaction (RT-PCR) were applied to detect the changes of EMT markers in vivo and in vitro, respectively. Results showed the expressions of TGF-β1 and its downstream proteins smad3/p-smad3 were greatly reduced in TXL group; meantime, TXL restored the expression of smad7. As a result, the expressions of collagen IV (Col IV) and fibronectin (FN) were significantly decreased in TXL group. In vivo, 24 h-UAER (24-hour urine albumin excretion ratio) and BUN (blood urea nitrogen) were decreased and Ccr (creatinine clearance ratio) was increased in TXL group compared with DN group. In summary, the present study demonstrates that TXL successfully inhibits TGF-β1-induced epithelial-to-mesenchymal transition in DN, which may account for the therapeutic efficacy in TXL-mediated renoprotection.
    Keywords Other systems of medicine ; RZ201-999
    Subject code 630
    Language English
    Publishing date 2014-01-01T00:00:00Z
    Publisher Hindawi Limited
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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