排序方式: 共有55条查询结果,搜索用时 15 毫秒
31.
Costa B 《化学与生物多样性》2007,4(8):1664-1677
Cannabis is one of the first plants used as medicine, and the notion that it has potentially valuable therapeutic properties is a matter of current debate. The isolation of its main constituent, Delta9-tetrahydrocannabinol (THC), and the discovery of the endocannabinoid system (cannabinoid receptors CB1 and CB2 and their endogenous ligands) made possible studies concerning the pharmacological activity of cannabinoids. This paper reviews some of the most-important findings in the field of THC pharmacology. Clinical trials, anecdotal reports, and experiments employing animal models strongly support the idea that THC and its derivatives exhibit a wide variety of therapeutic applications. However, the psychotropic effects observed in laboratory animals and the adverse reactions reported during human trials, as well as the risk of tolerance development and potential dependence, limit the application of THC in therapy. Nowadays, researchers focus on other therapeutic strategies by which the endocannabinoid system might be modulated to clinical advantage (inhibitor or activator of endocannabinoid biosynthesis, cellular uptake, or metabolism). However, emerging evidence highlights the beneficial effects of the whole cannabis extract over those observed with single components, indicating cannabis-based medicines as new perspective to revisit the pharmacology of this plant. 相似文献
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The mammalian body has a highly developed immune system which guards against continuous invading protein attacks and aims at preventing, attenuating or repairing the inflicted damage. It is conceivable that through evolution analogous biological protective systems have been evolved against non-protein attacks. There is emerging evidence that lipid endocannabinoid signaling through cannabinoid 2 (CB2) receptors may represent an example/part of such a protective system/armamentarium. Inflammation/tissue injury triggers rapid elevations in local endocannabinoid levels, which in turn regulate signaling responses in immune and other cells modulating their critical functions. Changes in endocannabinoid levels and/or CB2 receptor expressions have been reported in almost all diseases affecting humans, ranging from cardiovascular, gastrointestinal, liver, kidney, neurodegenerative, psychiatric, bone, skin, autoimmune, lung disorders to pain and cancer, and modulating CB2 receptor activity holds tremendous therapeutic potential in these pathologies. While CB2 receptor activation in general mediates immunosuppressive effects, which limit inflammation and associated tissue injury in large number of pathological conditions, in some disease states activation of the CB2 receptor may enhance or even trigger tissue damage, which will also be discussed alongside the protective actions of the CB2 receptor stimulation with endocannabinoids or synthetic agonists, and the possible biological mechanisms involved in these effects. 相似文献
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Abstract: The haemogram of Rhynocoris kumarii Ambrose and Livingstone comprises prohaemocytes, plasmatocytes, granular haemocytes, cystocytes and oenocytoids. The impact of five insecticides, viz. monocrotophos, dimethoate, methylparathion, quinalphos and endosulfan on the total haemocyte count (THC) and differential haemocyte counts (DHC) was studied. All of the insecticides except endosulfan initially reduced both prohaemocytes and plasmatocytes, increased the granular haemocytes, altered the percentage of cystocytes and oenocytoids and increased the total haemocyte count (THC). On the contrary, endosulfan initially increased the prohaemocytes and plasmatocytes, decreased the granular haemocytes and also the THC. The highest impact on the DHC and THC was caused by methylparathion and monocrotophos and the least impact by endosulfan. Hence, endosulfan is considered as the safest insecticide followed by dimethoate and quinalphos among these five insecticides to use with R. kumarii . 相似文献
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The objectives of study were (a) to determine alteration of feeding, glucose level and oxidative stress and (b) to investigate expression and localization of cannabinoid receptors in type‐2 diabetic rat pancreas treated with Δ9‐tetrahydrocannabinol (Δ9‐THC). Rats were randomly divided into four groups: control, Δ9‐THC, diabetes and diabetes + Δ9‐THC groups. Diabetic rats were treated with a single dose of nicotinamide (85 mg/kg) 15 min before injection of streptozotocin (65 mg/kg). Δ9‐THC was administered intraperitoneally at 3 mg/kg/day for 7 days. Body weights and blood glucose level of rats in all groups were measured on days 0, 7, 14 and 21. On day 15 after the Δ9‐THC injections, pancreatic tissues were removed. Blood glucose levels and body weights of diabetic rats treated with Δ9‐THC did not show statistically significant changes when compared with the diabetic animals on days 7, 14 and 21. Treatment with Δ9‐THC significantly increased pancreas glutathione levels, enzyme activities of superoxide dismutase and catalase in diabetes compared with non‐treatment diabetes group. The cannabinoid 1 receptor was found in islets, whereas the cannabinoid 2 receptor was found in pancreatic ducts. Their localization in cells was both nuclear and cytoplasmic. We can suggest that Δ9‐THC may be an important agent for the treatment of oxidative damages induced by diabetes. However, it must be supported with anti‐hyperglycaemic agents. Furthermore, the present study for the first time emphasizes that Δ9‐THC may improve pancreatic cells via cannabinoid receptors in diabetes. The aim of present study was to elucidate the effects of Δ9‐THC, a natural cannabinoid receptor agonist, on the expression and localization of cannabinoid receptors, and oxidative stress statue in type‐2 diabetic rat pancreas. Results demonstrate that the cannabinoid receptors are presented in both Langerhans islets and duct regions. The curative effects of Δ9‐THC can be occurred via activation of cannabinoid receptors in diabetic rat pancreas. Moreover, it may provide a protective effect against oxidative damage induced by diabetes. Thus, it is suggested that Δ9‐THC can be a candidate for therapeutic alternatives of diabetes symptoms. Copyright © 2014 John Wiley & Sons, Ltd. 相似文献
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Jian-An Xian An-Li WangChao-Xia Ye Xiao-Dan ChenWei-Na Wang 《Comparative biochemistry and physiology. Toxicology & pharmacology : CBP》2010,152(2):182-188
The aim of this study was to investigate the cellular toxicity of copper-induced injury to the black tiger shrimp Penaeus monodon. The 24 h, 48 h, 72 h and 96 h LC50 (median lethal concentration) of Cu2+ on P. monodon (11.63 ± 1.14 g) were found to be 3.49, 1.54, 0.73 and 0.40 mg L− 1, respectively. Total haemocyte count (THC), phagocytic activity, respiratory burst (RB), cytoplasmic free-Ca2+ (cf-Ca2+) concentration and apoptotic cell ratio of shrimp were determined after exposure to different concentrations of Cu2+ (0, 0.05, 0.5, 1.5 and 3.5 mg L− 1) for 0, 6, 12, 24 and 48 h. There was no significant effect on the analytic indicator of shrimp exposed to 0.05 mg L− 1 Cu2+. THC decreased after Cu-exposure to 0.5 mg L− 1 for 48 h, 1.5 mg L− 1 for 24 h and 3.5 mg L− 1 for 12 h. Phagocytic activity decreased in P. monodon following 48 h exposure to 3.5 mg L− 1 Cu2+. RB was induced after 6 h exposure to 0.5, 1.5 and 3.5 mg L− 1 Cu2+. cf-Ca2+ concentration increased after 48 h exposure to 0.5 mg L− 1 Cu2+, and 12 h exposure to 1.5 and 3.5 mg L− 1 Cu2+. The percentage of apoptotic cells increased to 9.5%, 16.3% and 18.6% respectively following 48 h exposure to 0.5, 1.5 and 3.5 mg L− 1 Cu2+. These results indicate that Cu can induce oxidative stress, elevation of cf-Ca2+ and cell apoptosis, and inhibit phagocytic activity in the shrimp P. monodon, and the lethal injury of Cu2+ to P. monodon may be mainly due to the sharp reduction of THC caused by ROS-induced apoptosis. 相似文献
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Autophagy and tumorigenesis 总被引:1,自引:0,他引:1
Nan Chen 《FEBS letters》2010,584(7):1427-674
Autophagy, or cellular self-digestion, is activated in cancer cells in response to multiple stresses and has been demonstrated to promote tumor cell survival and drug resistance. Nonetheless, genetic evidence supports that autophagy functions as a tumor suppressor mechanism. Hence, the precise role of autophagy during cancer progression and treatment is both tissue and context dependent. Here, we discuss our current understanding of the biological functions of autophagy during cancer development, overview how autophagy is regulated by cancer-associated signaling pathways, and review how autophagy inhibition is being exploited to improve clinical outcomes. 相似文献
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Unzicker C Erberich H Moldrich G Woldt H Bulla J Mechoulam R Ehrenreich H Sirén AL 《Neurochemical research》2005,30(10):1305-1309
Endothelin (ETB)-receptors mediate anti-apoptotic actions. Lack of functional ETB-receptors leads to increased neuronal apoptosis
in the hippocampus. The increased apoptosis must be compensated by other mechanisms, however, as ETB-deficient rats display
normal overall brain morphology. To illuminate on brain plasticity in ETB-receptor deficiency, we studied the expression and
function of another neuroprotective system, the cannabinoid CB1-receptors, in ETB-deficient hippocampus. We show that CB1
expression in hippocampus increases postnatally in all rats but that the increase in CB1-receptor expression is significantly
higher in ETB-deficient compared to wildtype littermates. Neuronal apoptosis decreases during brain maturation but remains
on a significantly higher level in the ETB-deficient compared to wildtype dentate. When investigating survival of hippocampal
neurons in culture, we found significant protection against hypoxia-induced cell death with CB1-analogs (noladin, (9-tetrahydrocannabinol)
only in ETB-deficient neurons. We suggest that CB1-receptor upregulation in the ETB-mutant hippocampus reflects an attempt
to compensate for the lack of ETB-receptors.
Special issue dedicated to Dr. Bernd Hamprecht 相似文献
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Cannabinoids are compounds that can modulate neuronal functions and immune responses via their activity at the CB1 receptor. We used 2H NMR order parameters and relaxation rate determination to delineate the behavior of magnetically aligned phospholipid bilayers in the presence of several structurally distinct cannabinoid ligands. THC (Δ9-Tetrahydrocannabinol) and WIN-55,212-2 were found to lower the phase transition temperature of the DMPC and to destabilize their acyl chains leading to a lower average SCD (≈ 0.13), while methanandamide and CP-55,940 exhibited unusual properties within the lipid bilayer resulting in a greater average SCD (≈ 0.14) at the top of the phospholipid upper chain. The CB1 antagonist AM281 had average SCD values that were higher than the pure DMPC lipids, indicating a stabilization of the lipid bilayer. R1Z versus |SCD|2 plots indicated that the membrane fluidity is increased in the presence of THC and WIN-55,212-2. The interaction of CP-55,940 with a variety of zwitterionic and charged membranes was also assessed. The unusual effect of CP-55,940 was present only in bicelles composed of DMPC. These studies strongly suggest that cannabinoid action on the membrane depends upon membrane composition as well as the structure of the cannabinoid ligands. 相似文献