Urinary metabolomics analysis to reveal metabolic mechanism of guanxinning injection on heart failure with renal dysfunction

Wang, Chun-liu; Li, Zhihao; Qi, Ling; Zhou, Jie; Wang, Shixiang; Xiao, Chaoni; Yang, Wenwen; Liang, Ji-ping; Wang, Fengyun; Yang, Yang; Zhou, Hong; Zhao, Ye; Li, Ye; Zheng, Xiaohui; Jia, Ping

doi:10.1016/j.jpba.2021.114516

Cited by 7 publications

(2 citation statements)

References 28 publications

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“…Although no changes in CREA and UREA were found in this study, another study revealed that GXN could reduce the elevation of blood UREA and serum cystatin C induced by transverse aortic constriction and alleviate renal pathological injury. Moreover, the metabolic mechanism of GXN in the treatment of HF with CRF by urinary metabolomics analysis showed that the cardiorenal protective mechanism of GXN was mainly related to energy metabolism and oxidative stress ( 26 ).…”

Section: Discussionmentioning

confidence: 99%

Guanxinning Injection Combined With Ischemic Postconditioning Attenuate Myocardial Ischemic Reperfusion Injury in Chronic Renal Failure Rats by Modulating Mitochondrial Dynamics

Wang

Zhang

Liu

et al. 2022

Front. Cardiovasc. Med.

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PurposeSalvia miltiorrhiza Bge. (Danshen, DS) and Ligusticum chuanxiong Hort. (Chuanxiong, CX) have been widely used in traditional Chinese medicine to prevent and treat myocardial ischemia and renal insufficiency, and their extracts (Guanxinning injection, GXN) have been reported to exhibit antioxidant, anti-inflammatory, and anti-ischemia-reperfusion injury properties. It is well-established that ischemic postconditioning (IPOC) can protect against myocardial ischemia-reperfusion (I/R) injury in rats with chronic renal failure (CRF). However, little is known on whether GXN combined with IPOC may affect myocardial I/R injury in CRF rats. We sought to observe the effect of GXN combined with IPOC on myocardial I/R injury in CRF rats by quantifying changes in the expression of proteins related to mitochondrial dynamics.Materials and MethodsIn a survey, 90 Wistar rats were randomly divided into 6 groups (15 rats per group): CRF group, I/R group, comorbid group (CRF + I/R), IPOC group, IPOC + GXN group and the sham group. Changes in blood myocardial injury markers, urea, and creatinine were analyzed. Heart tissues were harvested for histomorphometry and western blotting when rats were sacrificed. Myocardial infarction area was measured by Evans blue and Triphenyltetrazolium chloride solution staining. The expressions of mitochondrial fission relative proteins (DRP1 and FIS1) and mitochondrial fusion relative proteins (OPA1 and MFN1) were detected by western blotting.ResultsIPOC could significantly decrease myocardial injury markers and myocardial area of necrosis (AN)/area at risk (AAR) of the comorbid model rats. Further results showed that GXN combined with IPOC could significantly reduce CK-MB levels and myocardial AN/AAR in comorbid model rats compared with the IPOC group. Meanwhile, both IPOC and IPOC + GXN significantly reduced DRP1 levels and increased the MFN1 and OPA1 protein levels in the comorbid model rats. However, compared with the IPOC group, MFN1 and OPA1 protein levels increased significantly in the IPOC + GXN group.ConclusionExtracts of DS and CX combined with IPOC exert a protective effect against myocardial I/R injury in rats with CRF, mediated by increased expression of mitochondrial fusion proteins (MFN1 and OPA1).

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Section: Discussionmentioning

confidence: 99%

Guanxinning Injection Combined With Ischemic Postconditioning Attenuate Myocardial Ischemic Reperfusion Injury in Chronic Renal Failure Rats by Modulating Mitochondrial Dynamics

Wang

Zhang

Liu

et al. 2022

Front. Cardiovasc. Med.

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“…Increasing evidence suggests that taurine-induced neuroprotection is mediated by the antagonism of glutamate-induced excitotoxicity [14]. Taurine content was much higher in the model groups than the control group, possibly as a compensatory response to antioxidant damage [15,16]. Taurine content decreased after treatment with CK, thus indicating that CK decreased oxidative stress and eliminated the compensatory response.…”

Section: Highlightsmentioning

confidence: 93%

Protective effects of ginsenoside CK against oxidative stress-induced neuronal damage, assessed with 1H-NMR-based metabolomics

Zhang

et al. 2022

Acta Materia Medica

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Oxidative stress is an important pathogenic mechanism in degenerative diseases such as Alzheimer’s disease. Although ginsenoside compound K (CK) is protective against neuronal oxidative damage, the underlying mechanism remains to be understood. In this study, the protective effects of ginsenoside CK against oxidative stress damage induced by hydrogen peroxide in HT22 cells were investigated with 1H nuclear magnetic resonance (1H-NMR)-based metabolomics. The optimal CK concentration for decreasing oxidative stress damage in nerves was determined with MTT assays. CK (8 μM) significantly increased the HT22 cell survival rate after the model was established. Cell lysates were subjected to 1H-NMR metabolomics, western blotting, and ATP assays for verification. Metabolic perturbation occurred in HT22 cells in the model group but not the control group. Twenty biomarkers were identified and used to analyze metabolic pathways. CK reversed metabolic changes in HT22 cells by altering taurine, glutamate, glycine, and glutathione metabolism. Subsequently, CK increased ATP content and the expression of components of the PI3K/AKT signaling pathway in HT22 cells. These findings demonstrated that CK prevents oxidative stress damage and protects nerves by regulating energy-metabolism pathways, such as those of taurine, glutamate, and other amino acids, thus providing a rationale for the use of CK in Alzheimer’s disease treatment.

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Mechanism of XiJiaQi in the treatment of chronic heart failure: Integrated analysis by pharmacoinformatics, molecular dynamics simulation, and SPR validation

Zhao,

Guo,

Zhang

et al. 2023

Computers in Biology and Medicine

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Urinary metabolomics analysis to reveal metabolic mechanism of guanxinning injection on heart failure with renal dysfunction

Cited by 7 publications

References 28 publications

Guanxinning Injection Combined With Ischemic Postconditioning Attenuate Myocardial Ischemic Reperfusion Injury in Chronic Renal Failure Rats by Modulating Mitochondrial Dynamics

Guanxinning Injection Combined With Ischemic Postconditioning Attenuate Myocardial Ischemic Reperfusion Injury in Chronic Renal Failure Rats by Modulating Mitochondrial Dynamics

Protective effects of ginsenoside CK against oxidative stress-induced neuronal damage, assessed with 1H-NMR-based metabolomics

Mechanism of XiJiaQi in the treatment of chronic heart failure: Integrated analysis by pharmacoinformatics, molecular dynamics simulation, and SPR validation

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