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Background In neonatal rats, MK-801 treatments can produce schizophrenia-like symptoms. Crocin is a water soluble carotenoid in Saffron that exerts potent neuroprotective effects. This work aimed to demonstrate the function of crocin in the alleviation of motor and cognitive impairments elicited by MK-801 in a neonatal rodent schizophrenia model, and to illustrate the underlying molecular mechanisms. Methods Rats were treated with vehicle, MK-801 (1 mg/kg), MK-801 + 25 mg/kg crocin, or MK-801 + 50 mg/kg crocin. Motor learning and coordination, locomotion and exploratory activities, as well as spatial memory were assessed using the rotarod test, pen field test, and the Morris water maze test, respectively. Relative mRNA and protein levels of genes of interest were analyzed using qRT-PCR and Western blot assays, respectively. Results In the hippocampus of rats with MK-801-elicited schizophrenia, administration of crocin elevated the expression of silent information regulator-1 (SIRT1) and brain derived neurotrophic factor (BDNF), and relieved the oxidative stress. The learning deficits and motor perturbations caused by MK-801 treatments were also alleviated by the crocin administration. Conclusion Collectively, crocin has exerted neuroprotective effects in the rat model of MK-801-elicited schizophrenia, via regulations of SIRT1 and downstream BDNF expression in the hippocampus.

Background & Aims Tetrandrine (Tet) has been reported to have anti-inflammatory effects and protect from the ischemic strokes. The NLRP3 inflammasome plays a key role in cerebral ischemia/reperfusion (I/R)-induced inflammatory lesions. However, the molecular mechanisms of Tet related to the progression of cerebral ischemia are still unclear. Therefore, the aim of this study was to investigate the possible effects of Tet on cerebral ischemia and the related mechanisms involved in NLRP3 inflammasome. Methods C57BL/6J mice used as a cerebral I/R injury model underwent middle cerebral artery occlusion (MCAO) for 2 h following reperfusion for 24 h. Tet (30 mg/kg/day, i.p.) was administered for seven days and 30 min before and after MCAO. Their brain tissues were evaluated for NLRP3 inflammasome and Sirtuin-1 (Sirt-1) expression. An intracerebroventricular injection of Sirt-1 siRNA was administered to assess the activation of the NLRP3 inflammasome. Results Tet significantly reduced the neurological deficits, infarction volume, and cerebral water content in MCAO mice. Moreover, it inhibited I/R-induced over expression of NLRP3, cleaved caspase-1, interleukin (IL)-1β, IL-18, and Sirt-1. Sirt-1 knockdown with siRNA greatly blocked the Tet-induced reduction of neurological severity score and infarct volume, and reversed the inhibition of NLRP3 inflammasome activation. Conclusion Our results demonstrate that Tet has benefits for cerebral I/R injury, which are partially related to the suppression of NLRP3 inflammasome activation via upregulating Sirt-1.

The aim of this study was to assess the expression of Th17-associated gene, AMPs genes and SIRT-1 protein in patients with inflammatory bowel disease (IBD). Material and Methods: We studied a group of 20 IBD patients, together with 20 subjects served as controls. Colonoscopy, terminal ileoscopy, and colonoscopic biopsy were performed for histopathology diagnosis, and quantitative gene expression of Th17-associated gene, CAMP, Elafin and SLPI by real-time PCR. SIRT-1 protein level expression was assessed by western blot. Results: The expression of the four studied genes—elafin, SLPI, CAMP and Th17-associated gene—by relative quantification was higher in the patient group than in the control group. A statistically significant positive correlation was found between SLPI and elafin in the patient group (r= 0.8325 P

Dysregulated lipid profile with hypertriglyceridemia and increased low-density lipoprotein (LDL) is common in chronic kidney disease (CKD) whereas the reason is unclear. A similar phenomenon is found in the elder population. Silent information regulator-1 (SIRT1) associates with many modulators regulating lipid metabolism and results in increased expression of sterol regulatory element-binding proteins (SREBPs), which functions as a key modulator in lipid synthesis. Since CKD is being viewed as a premature aging model and SIRT1 is known to decrease during the process of aging, we hypothesize that SIRT1 level is reduced in the liver when CKD develops and eventually result in dysregulated lipid profile.