Regulation of antioxidant system, lipids and fatty acid ß-oxidation contributes to the cardioprotective effect of sodium tanshinone IIA sulphonate in isoproterenol-induced myocardial infarction in rats.

OBJECTIVE: Myocardial infarction (MI) is a cause of high morbidity and mortality in the world. Sodium tanshinone IIA sulphonate (STS) has been well used in Oriental medicine for treating cardiovascular diseases, however, the underlying mechanisms remain unclear. Alterations of circulating lipid profiles, increased fatty acid ß-oxidation and oxidative stress play most important roles in the pathogenesis of MI. The present study aims to elucidate whether STS possesses cardioprotective effect against MI driven by isoproterenol (ISO), and to investigate its potential mechanisms of action. METHODS: MI was induced by subcutaneous injection of ISO (85 mg/kg at interval of 24 h for 2 consecutive days) to rats. The rats were randomly divided into 6 groups: (1) control; (2) ISO; (3) STS (16 mg/kg) +control; (4-6) STS (16, 8, 4 mg/kg) +ISO. RESULTS: Our study showed that STS could ameliorate cardiac dysfunction and variation of myocardial zymogram, up-regulate antioxidant systems, and maintain the levels of circulating lipids driven by supramaximal doses ISO as well. Moreover, modulation of redox-sensitive extracellular signal-regulated kinase1/2 (ERK1/2)/Nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) and AMP-activated protein kinase (AMPK)/acetyl CoA carboxylase (ACC)/carnitine palmitoyltransferase (CPT) 1 pathways were involved in STS induced cardioprotection. CONCLUSIONS: STS exerts strong favorable cardioprotective action. Additionally, the properties of STS, such as anti-dyslipidemia, anti-oxidant and inhibition of fatty acid ß-oxidation, may be the mechanisms underlying the observed results.

Akebia Saponin D attenuates amyloid ß-induced cognitive deficits and inflammatory response in rats: involvement of Akt/NF-κB pathway.

Neuroinflammatory responses caused by amyloid ß(Aß) play an important role in the pathogenesis of Alzheimer's disease (AD). Aß is known to be directly responsible for the activation of glial cells and induction of apoptosis. Akebia Saponin D (ASD) is extracted from a traditional herbal medicine Dipsacus asper Wall, which has been shown to protect against ibotenic acid-induced cognitive deficits and cell death in rats. In this study, we investigated the in vivo protective effect of ASD on learning and memory impairment induced by bilateral intracerebroventricular injections of Aß1-42 using Morris water and Y-maze task. Furthermore, the anti-inflammatory activity and neuroprotective effect of ASD was examined with methods of histochemistry and biochemistry. These data showed that oral gavage with ASD at doses of 30, 90 and 270 mg/kg for 4 weeks exerted an improved effect on cognitive impairment. Subsequently, the ASD inhibited the activation of glial cells and the expression of tumor necrosis factor (TNF)-α, interleukin-1 beta (IL-1ß) and cyclooxygenase-2 (COX-2) in rat brain. Moreover, ASD afforded beneficial actions on inhibitions of Akt and IκB kinase (IKK) phosphorylations, as well as nuclear factor κB (NF-κB) activation induced by Aß1-42. These results suggest that ASD may be a potential agent for suppressing both Alzheimer's disease-related neuroinflammation and memory system dysfunction.