No abstract

Honokiol, a constituent extracted from Magnolia officinalis, had been shown be an antioxidant and an anti-platelet agent in biological systems with an anti-arrhythmic effect and a myocardial protective effect on ischemia-reperfusion injury. We examined the neuroprotective effect of honokiol in rats subjected to focal cerebral ischemia. Honokiol was administered intravenously either at fifteen minutes before right middle cerebral artery occlusion (pretreatment groups) or when both common carotid arteries clips were removed (treatment groups). The results showed that there was no significant hemodynamic change after intravenous infusion of honokiol at the dosages of 10(-8), 10(-7) and 10(-6) g/kg in both groups. However, honokiol significantly reduced the total volume of infarction at the doses of 10(-7) or 10(-6) g/kg in both pretreatment and treatment groups. This study suggests that honokiol is a potent neuroprotective agent in focal cerebral ischemia. This beneficial effect may be related to its antioxidant effect and anti-platelet aggregation activity.

No abstract

Organophosphorus flame retardants (OPFRs), a replacement for brominated flame retardants, have gradually been accepted as endocrine disrupting chemicals (EDCs). Recently, evidence has shown that these EDCs could cause chronic health problems, such as obesity, and referred to as metabolic disruptors. However, the disturbance to lipid metabolism caused by OPFRs remains poorly understood, especially at biological molecular levels. Herein, we used the human hepatocellular cells (HepG2) to study the lipid metabolism disruption caused by nine OPFRs (halogenated-, aryl-, and alkyl-containing). All the tested OPFRs, excluding the long carbon chain alkyl-OPFRs, could cause intracellular triglyceride (TG) and/or total cholesterol (TC) accumulation. In detail, aryl-OPFRs (TPhP and TCP) induced both TC and TG deposition. Halogenated-OPFRs (TCEP, TBPP, TDCPP, and TCPP) induced intracellular TG accumulation, and only TDCPP also induced TC accumulation. Furthermore, TPhP induced lipid accumulation through regulation genes encoding proteins involved in fatty acid β-oxidation, lipid, and fatty acid synthesis. All the halogenated-OPFRs cause TG accumulation only, enacted through β-oxidation rather than lipid synthesis. TPhP and TDCPP induced TC accumulation through both PPARγ and srebp2 signaling. Mitochondrial dysfunction including decreased oxygen consumption rate and ATP content may also contribute to lipid metabolic disruption by the tested OPFRs. Our data indicated that halogenated- and aryl-OPFRs may not be safe candidates, and further information should be made available as potential for, as well as the mechanism of, metabolic disruption. And long carbon chain alkyl-OPFRs may be safer than the other two groups.

No abstract