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Finally, we specify strategies with the potential to overcome the challenges that cannot be addressed via nanotechnology alone, including the alternative methods of TRAIL-expressing circulating cells, tumor-targeting bacteria, viruses, and exosomes. Renal ischemia-reperfusion (RI/R) injury with high morbidity and mortality is one common clinical disease. Development of drug targets to treat the disorder is critical important. MiR-27a-3p plays important roles in regulating oxidative stress. However, its effects on RI/R injury have not been reported. selleck compound In this paper, hypoxia/reoxygenation (H/R) models on NRK-52E and HK-2 cells, and RI/R model in C57BL/6 mice were established. The results showed that H/R in vitro decreased cell viability and increased ROS levels in cells, and RI/R caused renal injury and oxidative damage in mice. The expression levels of miR-27a-3p were up-regulated based on real-time PCR and FISH assays in model groups compared with control groups, which directly targeted Grb2 based on dual luciferase reporter assay and co-transfaction test. In addition, miR-27a- 3p markedly reduced Grb2 expression to down-regulate the expression levels of p-PI3K, p-AKT, Nrf2, HO-1, and up-regulate Keap1 expression in model groups. MiR-27a-3p mimics in vitro enhanced H/R-caused oxidative stress via increasing ROS levels and decreasing Grb2 expression to down-regulate PI3K-AKT signal. In contrary, miR-27a-3p inhibitor in vitro significantly reduced H/R-caused oxidative damage via decreasing ROS levels and increasing Grb2 expression to up-regulate PI3K-AKT signal. In vivo, miR-27a- 3p agomir exacerbated RI/R-caused renal damage by decreasing SOD level and increasing Cr, BUN, MDA levels via suppressing Grb2 expression to down-regulate PI3K- AKT signal. However, miR-27a -3p antagomir alleviated RI/R-caused oxidative damage via increasing Grb2 expression to up-regulate PI3k-AKT signal. Grb2siRNA in mice further enhanced RI/R-caused renal injury by increasing Cr, BUN, MDA levels and decreasing SOD level via inhibiting the expression levels of Grb2, Nrf2, HO-1, and increasing Keap1 expression. Our data showed that miR-27a-3p aggravated RI/R injury by promoting oxidative stress via targeting Grb2, which should be considered as one new drug target to treat RI/R injury. Cognitive psychologists have often discussed the idea that when Proust used in his books the concept of involuntary memories, which could be retrieved by an odor or a taste, he was in fact predating the notion of modern episodic memory. Since the publication of his famous "In Search of Lost Time", considerable progress has been made on our understanding of various types of memory and of the mechanisms involved in different brain circuits and synapses responsible for their long-term storage. This review will focus on the role of hippocampus in episodic memory, including its role in encoding time and various elements of episodes, in particular olfactory information. Our conclusion is that Proust did indeed predict the existence of episodic memory, although he did not realize that, in addition to remembering things past, memory is also used to predict the future. Our laboratory has investigated the role of an evolutionarily conserved RNA species called microRNAs (miRs) in regulation of anti-chlamydial protective immunity. MiRs including miR-155 expressed in specific immune effector cells are critical for antigen specific protective immunity and IFN-γ production. Using miR-155 deficient mice, and a murine pulmonary model for chlamydial infection, we report here 1) the effect of host miR-155 on bacterial burden, and 2) identify probable immune genes regulated by miR-155. ETHNOPHARMACOLOGICAL RELEVANCE The traditional Chinese medicine formula Danggui-Shaoyao-San (DSS) has been reported to show therapeutic effect on alleviating the symptoms of Alzheimer's disease (AD). AIM OF THE STUDY The present study aims to investigate the relation between DSS treatment of AD and DHA metabolism and evaluates its neuroprotective effect on cognitive in APP/PS1 mice. MATERIAL AND METHODS DSS (1.6, 3.2, 6.4 g/kg/day) or Aricept (3 mg/kg/day) was orally administered (i.g.) to APP/PS1 mice, and saline was orally administered to Wild-type (WT) male mice as control group. Then, the Morris water maze (MWM) test, Y-maze spontaneous alternation test, open filed test and fear conditioning test were conducted for evaluation of learning and memory abilities. The DHA content was assessed by HPLC-MS/MS. Physiological indices were determined, including triglyceride (TG), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), ROS level, activity of ppocampus as well as cortex of APP/PS1 mice. CONCLUSIONS Based on these results, we suggest that DSS play a positive effective role in increasing DHA content by up-regulating iPLA2 and 15-LOX, resulting in ameliorating oxidative stress and inflammation and finally ameliorating cognition deficits in APP/PS1 mice. ETHNOPHARMACOLOGICAL RELEVANCE Mao Dong Qing, the dry roots of Ilex pubescens Hook. et Arn, it has been often used for treating stroke and coronary artery disease. But whether IPEE treatment could promote cerebral ischemic tolerance (CIT) and induced endogenous neuroprotective effects to alleviate the nerve injury caused by the subsequent persistent cerebral ischemic attacks was unknown. AIM OF THE STUDY To investigate the effects of ethanol extracts of Ilex pubescens (IPEE)on enhancing CIT and explore the potential mechanisms. MATERIALS AND METHODS 108 adult male Wistar rats were employed in the present study. The bilateral common carotid arteries were blocked for 10 min, and then reperfusion were allowed for cerebral ischemic preconditioning (CIP); 3 days after CIP surgery, rats were subjected to middle cerebral artery occlusion/reperfusion (MCAO/R)-injury. Rats were continuous fed with IPEE for 5 days at the dose of 100 mg/kg or 200 mg/kg 24 h after the MCAO/R-injury, the brain infarct volume, histopatholomic tolerance by regulating the toll-like receptor 4 (TLR4) signaling pathway. The mechanisms of this response come in two primary forms inhibiting MyD88 dependent pro-inflammatory pathways and activating TRIF dependent anti-inflammatory pathways. V.