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Previous research has demonstrated that diabetes induces learning and memory deficits. However, the mechanism of memory impairment induced by diabetes is poorly understood. Dietary fatty acids, especially polyunsaturated fatty acids, have been shown to enhance learning and memory and prevent memory deficits in various experimental conditions. The present study investigated the effects of fish oil supplementation on the neuron apoptosis in the hippocampus of streptozotocin (STZ)-induced diabetes rats, further explored the effect of fish oil on the phosphorylation of protein kinase B and glycogen synthase kinase-3 beta. The effects of diabetes and fish oil treatment on the spatial learning and memory were also evaluated using the Morris Water Maze. STZ-induced diabetes impaired spatial learning and memory of rats, which was associated with the apoptosis of hippocampal neurons and oxidative stress. Fish oil administration ameliorated cognitive deficit, reduced oxidative stress, increased AKT phosphorylation, decreased GSK-3β phosphorylation, and decreased pro-apoptotic molecules expression, which protected the hippocampal neurons from apoptosis in diabetic rats. These results suggested a potential role for fish oil as an adjuvant therapy for the prevention and treatment of diabetic complications., (Copyright © 2014 Elsevier B.V. All rights reserved.)

Previous research has demonstrated that diabetes induces learning and memory deficits. However, the mechanism of memory impairment induced by diabetes is poorly understood. Dietary fatty acids, especially polyunsaturated fatty acids, have been shown to enhance learning and memory and prevent memory deficits in various experimental conditions. The present study investigated the effects of fish oil supplementation on the neuron apoptosis in the hippocampus of streptozotocin (STZ)-induced diabetes rats. The effects of diabetes and fish oil treatment on the spatial learning and memory were also evaluated using the Morris Water Maze. Diabetes impaired spatial learning and memory of rats. Diabetes increased the expression of Bax and caspase-3, which led the apoptosis of the CA1 pyramidal neurons, and further contributed to the deficits in learning and memory processing. Fish oil dietary supplementation in diabetic rats conducts neuron-protective function through an anti-apoptotic pathway and significantly improves the ability of learning and memory. These results partially explain the mechanism of the effect of diabetes and fish oil treatment on learning and memory, supporting a potential role for fish oil as an adjuvant therapy for the prevention and treatment of diabetic complications., (Copyright © 2012 Elsevier B.V. All rights reserved.)

Abstract: Previous research has demonstrated that diabetes induces learning and memory deficits. However, the mechanism of memory impairment induced by diabetes is poorly understood. The present study investigated the effect of streptozotocin (STZ)-induced diabetes on spatial learning and memory using the Morris Water Maze. The effects of diabetes on CA1 pyramidal neurons in hippocampus were also examined. Diabetes impaired spatial learning and memory of rats. Diabetes induced the apoptosis of neurons and translocation of Bax from cytoplasm to mitochondria. On the contrary, diabetes induced cytochrome c release into the cytoplasm from mitochondria. Release of Cyt-c from mitochondria into cytoplasm may play a role in apoptosis of the CA1 pyramidal neurons, which resulted in a decrease of the number of neurons in hippocampus and impaired the performance function. These results partially explain the mechanism of the effect of diabetes on learning and memory. To protect mitochondrial function is possible candidate for preventing the impairments of diabetes on hippocampal function. [Copyright &y& Elsevier]

Abstract As a continuation of our research on developing potent and potentially safe anti-proliferative agents, two series of novel Jiyuan Oridonin A-1,2,3-triazole-azole hybrids were designed, synthesized and evaluated for their anti-proliferative activity against four selected cancer cell lines (MGC-803, MCF-7, PC-3, Eca-109). Some compounds with better growth inhibitory effects were chosen to carry out further studies in A549 and SMMC-7721. Most of the synthesized compounds exhibited moderate to good activity against all the cancer cell lines selected. Particularly, the most active agent 8b showed high potency against human cancer cells with IC 50 ranging from 0.2 ± 0.0 to 5.0 ± 0.9 μM. Cellular mechanism studies elucidated compound 8b arrests cell cycle at G1 phase and induce a strong apoptotic response in SMMC-7721 cells. Furthermore, 8b could inhibit the colony formation and migration via Wnt signaling pathway in SMMC-7721 cells. For all these reasons, compound 8b holds promising potential as anti-proliferative agent. Graphical abstract A focused library of Jiyuan Oridonin A-1,2,3-triazole-azole derivatives were designed and synthesis. Compound 8b displayed the most potent inhibition against SMMC-7721 cells, inhibited colony formation and migration of SMMC-7721, as well as induced apoptosis. Image 1 Highlights • Jiyuan Oridonin A-1,2,3-triazole-azole hybrids inhibited proliferation of cancer cells. • Compound 8b exerted the most potent and broad-spectrum antiproliferative activity. • Compound 8b inhibited growth and migration of SMMC-7721 cells and induced apoptosis. [ABSTRACT FROM AUTHOR]