Changes in Plasma Lipid Levels and Antioxidant Activities in Rats after Supplementation of Obtusifolin.

Obtusifolin, an anthraquinone from Cassia obtusifolia seeds, has been reported to reduce blood lipid levels in diabetic rats induced by streptozocin. However, it remains unclear whether obtusifolin possesses a lipid-lowering effect on hyperlipidemia caused by a high-fat diet. Moreover, hyperlipidemia is known to impair the endothelial function by causing oxidative stress. Therefore, in the present study, we investigated the antidyslipidemic and antioxidant effects of obtusifolin in hyperlipidemic rats induced by a high-fat diet. Rats with oral fat emulsion were used as our hyperlipidemic model. We measured the body weight of the rats, serum total cholesterol, triglycerides, low-density lipoprotein cholesterol, and high-density lipoprotein cholesterol, as well as nitric oxide, malondialdehyde, and superoxide dismutase. Our results showed that oral obtusifolin application significantly reversed the changes induced by hyperlipidemia in body weight, total cholesterol, triglyceride, low-density lipoprotein cholesterol, and high-density lipoprotein cholesterol. Furthermore, obtusifolin treatment increased serum superoxide dismutase and nitric oxide, but reduced malondialdehyde. Collectively, our findings suggest that obtusifolin may improve hyperlipidemia by enhancing antioxidant activity. This study indicates a potential therapeutic importance of obtusifolin for ameliorating lipid dysfunction induced by a high-fat diet.

Cordycepin Ameliorates Synaptic Dysfunction and Dendrite Morphology Damage of Hippocampal CA1 via A1R in Cerebral Ischemia.

Cordycepin exerted significant neuroprotective effects and protected against cerebral ischemic damage. Learning and memory impairments after cerebral ischemia are common. Cordycepin has been proved to improve memory impairments induced by cerebral ischemia, but its underlying mechanism has not been revealed yet. The plasticity of synaptic structure and function is considered to be one of the neural mechanisms of learning and memory. Therefore, we investigated how cordycepin benefits dendritic morphology and synaptic transmission after cerebral ischemia and traced the related molecular mechanisms. The effects of cordycepin on the protection against ischemia were studied by using global cerebral ischemia (GCI) and oxygen-glucose deprivation (OGD) models. Behavioral long-term potentiation (LTP) and synaptic transmission were observed with electrophysiological recordings. The dendritic morphology and histological assessment were assessed by Golgi staining and hematoxylin-eosin (HE) staining, respectively. Adenosine A1 receptors (A1R) and adenosine A2A receptors (A2AR) were evaluated with western blotting. The results showed that cordycepin reduced the GCI-induced dendritic morphology scathing and behavioral LTP impairment in the hippocampal CA1 area, improved the learning and memory abilities, and up-regulated the level of A1R but not A2AR. In the in vitro experiments, cordycepin pre-perfusion could alleviate the hippocampal slices injury and synaptic transmission cripple induced by OGD, accompanied by increased adenosine content. In addition, the protective effect of cordycepin on OGD-induced synaptic transmission damage was eliminated by using an A1R antagonist instead of A2AR. These findings revealed that cordycepin alleviated synaptic dysfunction and dendritic injury in ischemic models by modulating A1R, which provides new insights into the pharmacological mechanisms of cordycepin for ameliorating cognitive impairment induced by cerebral ischemia.