50 research outputs found
Spinal Astrocytic Activation Is Involved in a Virally-Induced Rat Model of Neuropathic Pain
Postherpetic neuralgia (PHN), the most common complication of herpes zoster (HZ), plays a major role in decreased life quality of HZ patients. However, the neural mechanisms underlying PHN remain unclear. Here, using a PHN rat model at 2 weeks after varicella zoster virus infection, we found that spinal astrocytes were dramatically activated. The mechanical allodynia and spinal central sensitization were significantly attenuated by intrathecally injected L-α-aminoadipate (astrocytic specific inhibitor) whereas minocycline (microglial specific inhibitor) had no effect, which indicated that spinal astrocyte but not microglia contributed to the chronic pain in PHN rat. Further study was taken to investigate the molecular mechanism of astrocyte-incudced allodynia in PHN rat at post-infection 2 weeks. Results showed that nitric oxide (NO) produced by inducible nitric oxide synthase mediated the development of spinal astrocytic activation, and activated astrocytes dramatically increased interleukin-1β expression which induced N-methyl-D-aspartic acid receptor (NMDAR) phosphorylation in spinal dorsal horn neurons to strengthen pain transmission. Taken together, these results suggest that spinal activated astrocytes may be one of the most important factors in the pathophysiology of PHN and “NO-Astrocyte-Cytokine-NMDAR-Neuron” pathway may be the detailed neural mechanisms underlying PHN. Thus, inhibiting spinal astrocytic activation may represent a novel therapeutic strategy for clinical management of PHN
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Effects of Conjugated Linoleic Acid (CLA) on Differentiation of Murine Bone Marrow Stem Cells (Abstract)
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Direct Inhibition of Stearoyl-CoA Desaturase Activity by trans-10,cis-12 Conjugated Linoleic Acid
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Biological Activities of Conjugated Fatty Acids: Conjugated Eicosadienoic (conj. 20:2Δc11,t13/ t12,c14), Eicosatrienoic (conj. 20:3Δc8,t12,c14), and Heneicosadienoic (conj. 21:2Δc12,t14/ c13,t15) Acids and Other Metabolites of Conjugated Linoleic Acid
The elongated form of conjugated linoleic acid (CLA), conjugated eicosadienoic acid (CEA, conj. 20:2Δc11,t13/t12,c14), was generated from CLA by liver microsomal fractions. Subsequent testing showed that dietary CEA significantly reduced body fat, and increased lean mass similar to CLA when compared to controls. CEA also decreased lipoprotein lipase activity and triacylglyceride, and increased glycerol release in 3T3-L1 adipocytes, correlated with the trans-12,cis-14 isomer, but CEA required a longer incubation period than cells treated with CLA. Based on the fact that CEA fed animals had CLA in tissue, we suggest that the effect of CEA is due to the CLA converted from CEA in the system. The delta-6 desaturated and elongated form of trans-10,cis-12 CLA (conjugated eicosatrienoic acid, CETA, conj. 20:3Δc8,t12,c14) inhibited LPL activity and increased glycerol release but was less active than trans-10,cis-12 CLA or CEA. The 21-carbon conjugated fatty acid, conjugated heneicosadienoic acid (CHDA, conj. 21:2Δc12,t14/c13,t15), was not active on LPL inhibition, triacylglyceride, or glycerol release in 3T3-L1 adipocytes. We also provide evidence that CLA was metabolized to conjugated dodecadienoic acid (conj. 12:2Δc3,t5/t4,c6). In addition, there were indications of the presence of conjugated tetradecadienoic acid (conj. 14:2Δc5,t7/t6,c8), suggesting that CLA can be metabolized through fatty acid β-oxidation. This is the first work to report the presence of conjugated 12 and 14 carbon fatty acids, originated from CLA, and the biological activities of CEA, CETA and CHDA
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Trans-10,cis-12 Conjugated Linoleic Acid Inhibits Differentiation in 3T3-L1 Adipocytes and Decreases Peroxisome Proliferator-activated Receptor Expression in Mice (Abstracts)
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Effects of Dietary Conjugated Linoleic Acid (CLA) on Spontaneously Hypertensive Rats
Conjugated linoleic acid (CLA) is a mixture of positional and geometric isomers of linoleic acid found in beef, lamb, and dairy products. CLA has attracted considerable attention over the past several decades because of its potentially beneficial biologic effects, including protective effects against several cancers, atherosclerosis, and obesity. In previous studies, we provided evidence that dietary CLA could prevent the development of obesity-related hypertension in obese animals. Here, we show that CLA suppresses the development of non-obese essential hypertension in spontaneously hypertensive rats (SHRs). After 4 weeks of feeding with CLA, the increase of systolic blood pressure was significantly suppressed compared with rats fed linoleic acid. Abdominal adipose tissue weight was also significantly lowered in CLA-fed SHRs. Content of arachidonic acid, the substrate of eicosanoid production, was not changed, but accumulation of oleic acid, the lipogenesis end-product, was markedly decreased in the membrane phospholipids of CLA-fed SHRs. In addition, we found increased level of plasma adiponectin, suggested as a regulatory factor of hypertension, through the enhancement of mRNA expression in CLA-fed SHRs. We speculate that the antihypertensive effect of dietary CLA may be due to the increase of plasma adiponectin level and associated with the alleviation of membrane abnormality in SHRs
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Formation of Acrylamide in Potato Chip and French Fry Models (Book of Abstracts P.87)
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