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GW23-e0181
ANTI-INFLAMMATORY EFFECT OF GINSENOSIDE RG1 ON CARDIOMYOCYTE INJURY INDUCED BY ADRIAMYCIN
  1. Hongliang Kong,
  2. Hongliang Kong
  1. The People's Hospital of Liaoning Province

    Abstract

    Objectives Chronic inflammation have played an important role in heart failure (HF). Ginsenoside Rg1 (Gs-Rg1), stemming from Ginseng, is a kind of major pharmacologically active components. However, the effect of Gs-Rg1 in HF remains to being explored, let alone its mechanisms. Thus, the present study aimed at examining the effect of Gs-Rg1 in HF, and then further elucidates its effects on proinflammatory factor, such as tumour necrosis factor alpha (TNFα), and nuclear transcription factor kappa B (NF-кB) basing on rat HF model induced by adriamycin, in vivo.

    Methods Rat with adriamycin-induced HF were randomly divided into control group (age-matched health rat, n=15), HF group (ie, adriamycin group, n=15), Gs-Rg1 group (Gs-Rg1 intervention basing on HF, n=15), Gs-Rg1 was intraperitoneally administered according to body weight (4 mg/100 g) once a day for 14 days. Left ventricular ejection fraction (LVEF) was estimated through echocardiographic examination, the above gene and the above protein was estimated through ELISA, real-time RT-PCR, western blot and Electrophoretic mobility shift assay.

    Results 1. Gs-Rg1 significantly improved LVEF (p=0.005).

    2. Both protein and mRNA of TNFα and TNFR-1 in the HF group were higher than that in the control group (all p<0.001), which were markedly reduced by Gs-Rg1 (all p<0.001).

    3. Gs-Rg1 augmented protein and mRNA of TNFR-2, which was lower in HF group than in control group.

    4. Compared to HF group, Gs-Rg1 markedly inhibited the protein level of total-IKKα, phospho-IKKα, total-IKKβ and phospho-IKKβ, including their IKKα phosporylation (ie, the ratio of phosphorylated to total protein) and IKKβ phosporylation (all p<0.001).

    5. Treatment with Gs-Rb1 caused a significant increase in total-IκB and IκB, and a significant decrease in IκB phosporylation compared with HF group (all p<0.01).

    6. Gs-Rb1 markedly decreased total-NF-кB protein, phospho-NF-кB protein and NF-кB mRNA than that in HF group (all p<0.01).

    Conclusions Gs-Rg1 may improve HF, which was mediated by proinflammatory factors, including a decrease in TNFα, NF-κB and an increase in both TNFR-2 and IκB.

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