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Introduction @#In recent years, there has been a significant increase of cerebrovascular disease in Mongolia, which is the second leading cause of mortality. There are dozens of Mongolian traditional medicine which is good efficiency for cerebral ischemia that contains musk.@*Aim@#Therefore, we aimed to investigate the effect of musk under the cerebral ischemia/reperfusion in rats.@*Materials and Methods@#Cerebral middle cerebral artery occlusion was established in male rat (90-minute occlusion followed by 24-hour reperfusion). Rats were divided into following groups: control group, ischemia group (cerebral ischemia and reperfusion), nimodipine administrated group (cerebral ischemia and reperfusion + treated with nimodipine), musk administrated group (cerebral ischemia and reperfusion + musk 50 mg/kg and 100 mg/kg). The brain tissue levels of IL-1β, TNF-α, IL-6, IL-10 cytokines were measured using enzyme linked immunosorbent assay (ELISA) every 1, 3, 7th days.@*Results@#Levels of cytokines (IL-1β, TNF-α and IL-6) were significantly lower in musk treated group compared to brain ischemia group (p<0.05). In contrast, treatment with musk was significantly improved neurological function with stimulation of M2 phenotype microglia cells and increased the anti-inflammatory cytokine level of IL-10 in the ischemic hemisphere of brain in rats@*Conclusion@#The mechanisms of musk are associated with increasing the brain tissue levels of IL-10, and reducing the levels of proinflammatory cytokines such as IL-1β, TNF-α, IL-6 subsequently stimulating neurogenesis and reduced ischemic zone. Musk may have neuroprotective effects against cerebral ischemia with stimulating M2 phenotype microglia cells in the brain. Regarding the ELISA, the effects of musk may be due to anti-inflammatory properties through inhibition of some of proinflammatory cytokines and stimulation of anti- inflammatory cytokines.
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INTRODUCTION:Alcohol (EtOH) use disorders (AUDs) represent a substantial public health problem worldwide. Over 76million people present with AUDs 2.5 million deaths were attributed to alcohol (World Health Organization,2010). Channadshelshi has been used for treatment of alcohol-related, liver disease and intoxication intraditional medicine.GOAL:To determine effect of channadshelshi on voluntary alcoholic wistar rats.MATERIALS AND METHODS:To examine acute toxicity of Channadselshi were used V.P.Prozorovsky express method (1978) andOECD (2001).Voluntary EtoH consumption measurement (two-bottle choice, intermittent access to EtOH paradigm inwistar rats). Water and 20% ethanol were presented in 200 mlgraduated plastic cylinders with stainlesssteeldrinking spouts.The experiment period was 10 weeks total. EtOH consumption was expressed asgrams of EtOH consumed per kilogram of body weight/day.Elevated plus maze. Anxiety associated with EtoH withdrawalwas measured on EPM The mazewaselevated 1 m above the floor and contained four 50 cm long, 10 cmwidearms arranged at rightangles. The closed arms had opaque walls 30cm high, extending the length of the arm. At the time of thetest, eachanimal was placed in the center of the maze facing an open arm andallowed to explore for a5 min session. During this 5 min test session, theanimal’s number of arm entries and time spent in eacharm per entry was recorded on a camera.Pentylenetetrazol (PTZ) 100 mg/kg dose used in this study was determined as the dose that inducedseizures and protection against mortality in miceThe experimental protocol was approved by the Ethics Committee of the MNUMS. (№ 14-11/1À)RESULTS:LD50 of Channadselshi extract was found to be LD50=2.58 (2.1-3.2) gr/kg by V.P.Prozorovsky expressmethod (1978). Channadselshi was no acute toxic by OECD (2001).Ten and four weeks oral administration of Channadselshi (200 mg/kg) significantly (P<0.01) decreasedthe consumption of ethanol and significantly (P<0.01) increased time spent in open arm (EPM) involuntary alcoholic wistar rat compare to control.The time (sec) of latency the generalized convulsion were significantly (P<0.01) increased ofChannadselshi compare to control. The percent of protection against mortality were 80% in PTZinduced seizure in mice.CONCLUSIONS:1. Our study showed that Channadselshi hasreduced consumption of ethanol in voluntary alcoholicwistar rat.2. Channadselshi has central nervous system protection effect against PTZ induced seizure in mice.
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Snake venom toxins have been reportedly used as a rich source of a number of proteins of biotechnological interest due to their wide range of effects on haemostasis. These effects vary greatly: coagulant, anticoagulant, platelet-activating, anti-platelet, fibrinolytic and hemorrhagic, in either enzymatic or non-enzymatic pathways. Agkistrodon venom contains a variety of proteins that possess antiplatelet activities. This study presents recent development in our laboratory to produce and purify antiplatelet proteins derived from Agkistrodon blomhoffi ussuriensiss nake venom. Different matrices of HPLC (size exclusion, ion exchange and affinity chromatography) were employed for purifying the proteins and their biological and biochemical properties were characterized by SDSPAGE, 2-D electrophoresis, platelet aggregation assay and enzyme activity assay.A purified disintegrin was a single chain glycoprotein with Mr of 13 kDа and рІ 4.7, whereas PLA2 had Mr of 14 kDa and pI of 4.17. A dose-dependent activity curve analysis shows that the platelet aggregation inhibitory activity of disintegrin and PLA2 in the rabbit plateletrich plasma were ID50 of 0.25 μМ and 0.65 μМ, respectively. Bioprocesses to produce and purify active antiplatelet agents from A. blomhoffi ussuriensis venom have been developed, using modern liquid chromatography matrices. Ongoing work to optimize large-scale production process is being undertaken.