Songling Xuemaikang Capsule inhibits isoproterenol-induced cardiac hypertrophy via CaMKIIdelta and ERK1/2 pathways.
ERK1/2; Cardiac hypertrophy; Isoproterenol; CaMKIIdelta; Songling xuemaikang capsule; CaMKIIδ
ETHNOPHARMACOLOGICAL RELEVANCE: Cardiac hypertrophy is a key pathologic process in heart failure. Songling Xuemaikang Capsule (SXC), is a formulae of Chinese Medicine commonly used in China to treat hypertension and heart failure. However, its mechanism of effects on cardiac hypertrophy is still unclear. AIM OF THE STUDY: The aims of the present study were to investigate the cardio-protection roles and detailed mechanisms of SXC on cardiac hypertrophy in vivo and in vitro. MATERIALS AND METHODS: A rat model of cardiac hypertrophy was constructed by isoproterenol (ISO) intraperitoneal injection (i.p), 10 mg/kg/day for 3 days, and 4 groups were compared: CON (n = 8), ISO (n = 8), MET (metoprolol, positive drug treatment, n = 7), and SXC (SXC treatment, n = 6). Cardiac structure and function were evaluated with echocardiography in vivo. Dose-dependent curve was obtained with SXC different concentrations. In addition, H9C2 rat cardiomyocytes were cultured in vitro and the phosphorylation of ERK1/2, p38, JNK, AKT, and protein expression of CaN, CaMKIIdelta, GATA4 were detected with Western blot test. RESULTS: The results showed that SXC reduced diastolic thickness of left ventricular posterior wall, while did not change ejection fraction and fraction shortening significantly (P > 0.05). SXC inhibit ISO-induced cardiac hypertrophy dose-dependently with 50% inhibiting concentration (IC50) is 0.504 g/kg/day. Moreover, SXC inhibited the protein expression of CaMKIIdelta, and the phosphorylation of ERK1/2, so inhibiting protein expression of GATA4 in nucleus, and brain natriuretic peptide in serum (P < 0.001). CONCLUSION: The mechanism of SXC in the treatment of heart diseases involves SXC dose-dependently inhibited the ISO-induced cardiac hypertrophy via inhibiting CaMKIIdelta and ERK1/2/GATA4 signaling pathway.
Qi Jianyong; Tan Yafang; Fan Dancai; Pan Wenjun; Yu Juan; Xu Wen; Wu Jiashin; Zhang Minzhou
Journal of ethnopharmacology
2020
2020-02
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Journal Article
<a href="http://doi.org/10.1016/j.jep.2020.112660" target="_blank" rel="noreferrer noopener">10.1016/j.jep.2020.112660</a>
Protective Effects Of Ginsenoside Rg(2) Against Glutamate-induced Neurotoxicity In Pc12 Cells
Alzheimer's disease; apoptosis; beta peptide; calpain; damage; excitotoxicity; expression; Integrative & Complementary; ischemic neuronal death; Medicine; neuroprotection; nitric-oxide; Panax ginseng; Panax ginseng; Pharmacology & Pharmacy; Plant Sciences; receptors; system
We investigated the effect of ginsenoside Rg(2) on neurotoxic activities induced by glutamate in PC12 cells. The cells were incubated with glutamate (1 mmol/L), glutamate and ginsenoside Rg(2) (0.05, 0.1, 0.2 mmol/L) or nimodipine (5 mu mol/L for 24 h. The cellular viability was assessed by MTT assay. The lipid peroxidation products malondialdehyde (MDA) and nitrogen oxide (NO) were measured by a spectrophotometric method. Fura2/AM, as a cell permeable fluorescent probe for Ca2+, was used to detect intracellular Ca2+ concentration ([Ca2+](i)) using a monespectrofluorometer. Immunocytochemical techniques were employed to check the protein expression levels of calpain II, caspase-3 and beta-amyloid (A beta)1-40 in PC12 cells. The results showed that glutamate decreased the cell viability, increased [Ca2+](i), lipid peroxidation (the excessive production of MDA, NO) and the protein expression levels of calpain II, caspase-3 and A beta 1-40 in PC12 cells. Ginsenoside Rg(2) significantly attenuated glutamate-induced neurotoxic effects upon these parameters at all doses tested. Our study suggests that ginsenoside Rg(2) has a neuroprotective effect against glutamate-induced neurotoxicity through mechanisms related to anti-oxidation and anti-apoptosis. In addition, the inhibitory effect of ginsenoside Rg(2) against the formation of A beta 1-40 suggests that ginsenoside Rg(2) may also represent a potential treatment strategy for Alzheimer's disease. (c) 2007 Elsevier Ireland Ltd. All rights reserved.
Li N; Liu B; Dluzen D E; Jin Y
Journal of Ethnopharmacology
2007
2007-05
Journal Article or Conference Abstract Publication
<a href="http://doi.org/10.1016/j.jep.2006.12.015" target="_blank" rel="noreferrer noopener">10.1016/j.jep.2006.12.015</a>