There is evidence that inflammation and oxidative stress contribute to the neurodegenerative changes observed in Parkinson's disease. Unfortunately, there is a lack of curative treatment for this debilitating movement disorder. Boswellic acids (BAs) are pentacyclic triterpene molecules of plant origin that have been utilized for treating many inflammatory conditions. The current study was conducted to explore the protective role of BAs against rotenone-induced experimental parkinsonism. Twenty-four rats were assigned to one of four treatment groups. The first two groups were a vehicle group (no rotenone) and a rotenone control group in which rats received rotenone (1 mg/kg) every 48 h. The next 2 groups received rotenone (1 mg/kg every 48 h) plus protective oral doses of BAs (125 or 250 mg/kg daily). Rats in the rotenone group showed motor dysfunction when tested in the open-field arena and cylinder and rotarod tests. Moreover, inflammatory markers increased, whereas the dopamine level was lower in the striata of rats in the rotenone group versus those in the vehicle group. BAs taken by rats with rotenone-induced parkinsonism showed enhanced general motor performance, reduced inflammatory markers, and increased striatal dopamine level and nigral tyrosine hydroxylase immunostaining. In conclusion, BAs are promising agents in slowing the progression of Parkinson's disease if appropriate data become available about their safety and efficacy in humans.

Diabetes increases the sensitivity of myocardium to ischemic damage and impairs response of the myocardium to cardioprotective interventions. The present study aimed to elucidate the potential cardioprotective effect provided by ranolazine during myocardial infarction in nondiabetic and diabetic male rats. As AMP-activated protein kinase (AMPK) has been shown to be involved in the cellular response to ischemic injury, in this context, the present animal study evaluated the modulating role of ranolazine in the AMPK expression in isoprenaline-induced myocardial ischemic rat model. Male rats were divided into 2 experiments: experiment I and II (nondiabetic and diabetic rats) and assigned to normal control, saline control for isoprenaline, isoprenaline control, and ranolazine-treated groups. Ranolazine administration revealed effectiveness in attenuating the severity of isoprenaline-induced myocardial injury in both nondiabetic and diabetic rats as revealed by ECG signs, histopathological score, and apoptotic markers via abrogating the increments in the inflammatory and oxidative stress markers and modulating AMPK expression. Therefore, the current cardioprotective effect of ranolazine was, at least in part, mediated through inhibition of apoptosis and modulation of AMPK expression, encouraging considering the utility of ranolazine in protection from acute myocardial infarction.

Doxorubicin (DOX) is a potent chemotherapeutic agent. Unfortunately, due to the incidence of dose-dependent cardiotoxicity, its clinical usage is hampered. Natural products are gaining popularity as a means of preventing DOX-induced cardiotoxicity. In the present study, we investigated the cardiotoxic effects of DOX and assessed the potential ameliorative effects of Achillea fragrantissima extract, its combined ethyl acetate/ n. butanol (EtOAc-Bu) fraction, and vitamin E in adult male albino rats. Rats were randomly divided into five groups: Control, DOX, DOX + A. fragrantissima crude extract, DOX + its (EtOAc-Bu) fraction, DOX + Vitamin E. A single dose of DOX (15 mg/kg) was given intraperitoneally (ip) in each group except the control.Rats were assessed before scarification for arterial blood pressure and ECG recordings. Serum and heart tissue were collected for biochemical, and histopathological assessment. Pre-treatment with vitamin E, 0A. fragrantissima crude extract, and its (EtOAc-Bu) fraction ameliorated DOXinduced cardiotoxicity, in varying degrees and with varying significance, as evidenced by reversing the DOX-induced ECG changes, reducing serum cardiac enzymes, and improving DOX-induced histopathological changes. All the suggested protective measures, in varying degrees and with varying significance, reduced the oxidative stress, lipid peroxidation, and apoptosis markers (reduced NO, and MDA, down-regulated mRNA expression of both iNOS and caspase-3), and elevated the antioxidants markers (GR, SOD, and TAC). We concluded that such suggested natural products might offer a promising chemo-preventive approach against cardiotoxicity induced by DOX.

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