A comprehensive review on regulatory effects of crocin on ischemia/reperfusion injury in multiple organs.

Ischemia-reperfusion (I/R) injury affects o2-dependent organs including liver, kidneys, heart, brain, and intestine. I/R injury is described as the cellular injury in an organ caused by ischemia and then further aggravated during the reperfusion due to intracellular alterations. It is a process that happens in clinical settings such as organ transplantation, reperfusion after thrombolytic therapy, and coronary angioplasty. Crocus sativus L. known as saffron used in folk medicine for its beneficial effects. It contains multiple bioactive compounds including the crocin, crocetin, picrocrocin, and safranal. Crocin, a water-soluble carotenoid has antitumor, radical scavenging, anti hyperlipidemia and memory improving effects. Moreover, crocin has antioxidant, and protective effects on I/R models in rats at various organs such as heart, brain, kidney, stomach, liver, and kidney as described in detail in this review.

Central and peripheral administrations of levothyroxine improved memory performance and amplified brain electrical activity in the rat model of Alzheimer's disease.

Alzheimer's disease (AD) is associated with cognitive impairments and a decline in the spontaneous neuronal discharge. In the current study, we evaluated the effect of subcutaneous (S.C.) and intrahippocampal (I.H.) administrations of levothyroxine (LT-4) on the passive avoidance and spatial memory, as well as electrophysiological activity in an animal model of AD. One hundred-sixty male Wistar rats were divided into two main groups. The S.C. group included two Sham and four AD (vehicle or L-T4 25, 50 & 100µg/kg); and the I.H. had consisted of two Sham and two AD (vehicle or L-T4 10µg/kg) subgroups. To make an animal model of AD, amyloid beta (Aß) plus ibotenic acid (Ibo) were injected I.H. Rats were treated with L-T4 and/or normal saline for ten days. Passive avoidance and spatial memory were evaluated in shuttle box and Morris water maze, respectively. Neuronal single unit recording was assessed from hippocampal dentate gyrus (DG). Results showed that the mean latency time (s) increased significantly (p<0.001) in AD animals and decreased significantly in both S.C. and I.H. L-T4 injected AD animals, compared with the AD group (p<0.001). The percentage of total time that animals spent in goal quarter and the step through latency decreased significantly in AD rats (p<0.001) and increased significantly in both S.C. and I.H. L-T4 injected AD animals in comparison with the AD group (p<0.01, p<0.001). Data showed that the average number of spikes/bin significantly decreased in the AD group (p<0.001). The S.C. and I.H. L-T4 injections in AD rats significantly increased the spike rate in comparison to the AD group (p<0.001). In conclusion, both S.C. and I.H. injections of L-T4 alleviated memory deficits and spontaneous neuronal activity in Aß-induced AD rats. Also, I.H. microinjection of L-T4 had more beneficial effects on memory and neuronal electrophysiological activity in comparison to S.C. administration.

The protective activity of noscapine on renal ischemia-reperfusion injury in male Wistar rat.

OBJECTIVES: Bradykinin is a part of the kinin-kallikrein system which is involved in ischemia-reperfusion injury via B1 and B2 receptors. Noscapine is a non-competitive antagonist of bradykinin receptors. Noscapine has been reported to to be able to protect some organs against ischemia-reperfusion injury but its effect on renal ischemia-reperfusion injury (RIR) in rats is unknown. Therefore, the present study was designed to evaluate the effect of noscapine on renal ischemia-reperfusion injury in rats. MATERIALS AND METHODS: Twenty four rats were randomly assigned to four groups; sham, RIR control, pre-and post-treatment with noscapine. To induce RIR injury, 20 days after right nephrectomy, animals underwent a midline laparotomy and the renal artery was clamped for 40 min to induce ischemia, and the clamp was then removed to allow reperfusion for 48 hr. Animals received noscapine or vehicle 1 hr before RIR or just prior to reperfusion. At the end of the experiment, animals were killed by cardiac exsanguination. Blood samples were collected to assess blood urea nitrogen (BUN) and creatinine. The kidneys were also removed for histopathlogical and western-blot analysis. RESULTS: Noscapine treatment 1 hr before RIR or just prior to reperfusion protects the renal tissue structure as compared with the control. The expression levels of the studied inflammatory mediators, TNF-α and MCP-1in pretreated-, and treated-noscapine groups decreased as compared with the control group. The levels of BUN and creatinine in pre-, and post-treated noscapine groups were significantly lower than in control animals. CONCLUSION: Noscapine protects renal tissue structure and function against RIR through down-regulation of the inflammatory mediators.