[Inhibitory effects of ethanolic extract of Cyperus rotandus on acetylcholinesrerase activity]

Background and Aim: Dementia is a progressive decline in mental and cognitive abilities which may be caused by brain injury or disease. Among several types of dementia, Alzheimer disease [AD] is the most prevalent. Acetylcholine is one of the mediators in brain which has a key role in recording, maintenance and recall of information in the brain. Neuronal cells secreting acetylcholine are among the first cells which are injured in Alzheimer disease. Prevention of degradation of acetylcholine by inhibition of acetylcholinesrerase can be essential for maintenance of memory and thinking. Considering increasing need for medicines with fewer side effects for the treatment of diseases such as AD, in this study we investigated the inhibitory effect of an extract of the Cyperus rotandus on the activity of acetylcholinestras

Material and Methods: Activity of the enzyme acetylcholinesterase [AchE] was measured by Ellman method, using Scale. Then, Lineweaver Burk plot was used to calculate Km, V[max] and Ki. In all the phases, the enzyme concentration was constant and its activity was measured in six different concentrations of acetylthiocholine [5, 10, 15, 20, 25 and 30 mM] at room temperature [25degree- 27degree C] based on optical absorption at 412 nm wavelength. Experiments were conducted in the presence of various concentrations ofphysostigmine [5.0, 75/0, 1, 1.5 and 2 mg/100ml] and Cyperus rotandus [1.0, 2.0, 3.0, 4.0, 5.0, 6.0 and 7/0 mg / ml]. Finally, according to Dixon plot we used different levels of inhibitor concentration and activity percentages to calculate IC[50] of inhibitors

Results: Ki of Cyperus rotandus was found to be almost 40 times greater than Ki of physostigmine. Values of IC[50] of physostigmine and Cyperusrotandus were 2.21 and mug/ml and 139 and mug/ml, respectively

Conclusion: Considering the mechanism of enzyme inhibitory effect, lower levels of Ki and IC[50] will lead to higher inhibitory effects. Therefore, the results showed that physostigmine was a stronger inhibitor compared to Cyperus rotandus. Moreover, with purification of the extract, higher inhibitory effects could be expected. In addition, Cyperus rotandus does not have the side effects such as nausea, vertigo, etc. which can be produced by physostigmine

Endothelium-dependent effect of sesame seed feeding on vascular reactivity of streptozotocin-diabetic rats: underlying mechanisms

Cardiovascular disorders continue to constitute major causes of morbidity and mortality in diabetic patients. In this study, the effect of chronic administration of sesame [Sesamum indicum L] seed feeding was studied on aortic reactivity of streptozotocin [STZ]-diabetic rats. Male diabetic rats received sesame seed-mixed food at weight ratios of 3% and 6% for 7 weeks, one week after diabetes induction. Contractile responses to KCl and phenylephrine [PE] and relaxation response to acetylcholine [ACh] and sodium nitroprusside [SNP] were obtained from aortic rings. Maximum contractile response of endothelium-intact rings to PE was significantly lower in sesame-treated diabetic rats [at a ratio of 6%] relative to untreated diabetics and endothelium removal abolished this difference. Endothelium-dependent relaxation to ACh was also significantly higher in sesame-treated diabetic rats [at a ratio of 6%] as compared to diabetic rats and pretreatment of rings with nitric oxide synthase inhibitor, N[G]-nitro-l-arginine methyl ester [L-NAME] significantly attenuated the observed response. Two-month diabetes also resulted in an elevation of malondialdehyde [MDA] and decreased superoxide dismutase [SOD] activity and sesame treatment significantly reversed the increased MDA content and restored activity of SOD. We thus conclude that chronic treatment of diabetic rats with sesame seed could in a dose- manner prevent some abnormal changes in vascular reactivity through nitric oxide and via attenuation of oxidative stress in aortic tissue and endothelium integrity is necessary for this beneficial effect

Evaluation of autoantibody against modified LDL levels in patients with cardioovascular diseases

Atherosclrosis is a process that initiated with hypercholestrolemia and fatty streak formation. Previous studies showed oxidative modification of LDL render immunogenic and autoantibodies to epitopes of oxidized LDL. Oxidized LDL [OX-LDL], has antigenic properties. Antibodies against oxidized LDL have been proposed to be independent predictors of atherosclerosis development. The main aims of the current study were to compare antibody titers to different types of oxidized LDL [Cu+2-LDL, Malondialdehyde-LDL] and Native-LDL between angiographically documented coronary patients, non-documented patients and healthy subjects. Correlation between autoantibodies against oxidized LDL and increased risks of cardiovascular diseases has been shown. As a case-control study, we evaluated angiographically documented coronary patients, non-documented patients and healthy subjects to measure anti-OX-LDL autoantibody levels. Enzyme-linked immunosorbent assay was used to measure anti-OX-LDL autoantibodies. ANOVA test used for statistical analysis. Titers of anti-Malondialdehydo-LDL autoantibodies were 3.55 +/- 0.415, 0.361 +/- 0.20, 0.093 +/- 0.078 respectively in each group [P<0.005]. There was not statistically meaningful difference, between native-LDL and Cu+2-LDL antibodies. It seems the titre of autoantibodies against OX-LDL considered as a predictor of progression of atherosclerosis. Our data provide further support for a role of oxidatively modified LDL in atherogenesis

[Comparing efficacy of two different hormonal therapy regimen on activity of coagulation factors VII, VIII, IX and serum lipids in menopaused women]

Background: during extrinsic coagulation pathway, a complex is developed between factor VII, calcium and tissue factor [a cell membrane lipoprotein that is exposed after cell injury]. Factor VII needs calcium and vitamin K for its biologic activation. Coronary artery disease can be induced by increased level and activity of the coagulation factors VII, VIII and IX. In postmenopausal period, estrogen can decrease blood lipids and thereby decreases risk of coronary artery disease. However, the exact effects of the estrogen on the other predisposing factors of the coronary artery diseases are unknown. Our objective in this study was to evaluate the effects of oral hormone therapy regimen on fibrinogen and other coagulation factors

Methods: 60 menopause women with history of hysterectomy were randomly allocated in 2 groups. One group was treated with conjugated estrogen 0.625mg/day and the other group was treated with conjugated estrogen 0.625mg/day and medroxy progesterone 2.5mg/day. Serum fibrinogen level and activity of coagulation factors VII, VIII and IX and blood lipids level were checked before and 3 months after treatment

Results: in the estrogen alone treated group, mean of factor VII activity showed significant elevation 3 months after treatment as compared with prior to hormone therapy[p<0.05]. There were no significant changes in means of coagulation factors VIII, IX activities and serum fibrinogen level in estrogen medroxy progesterone treated patients before and after treatment [p>0.05]. In both groups, honi1one therapy significantly decreased serum cholesterol level and LDL-C and increased HDL-C [p>0.00] but the serum triglyceride level was increased in the estrogen alone treated group

Conclusion: significant elevation of coagulation factors VII with significant elevation of serum triglyceride in estrogen treated patients is explainable. This study confirms that hormone therapy with this protocol does not change serum fibrinogen mean and activity of coagulation factor VIII and IX. This finding may be real or may be related to inadequacy of samples regarding the wide normal range of coagulation factors and serum fibrinogen. Studies with more prolonged follow-up or more samples are suggested