Effect of short and long-term treatment with omega-3 fatty acids on scopolamine-induced amnesia

Two omega-3 fatty acids including docosahexaenoic acid [DHA] and eicosapentaenoic acid [EPA] are essential for the physiologic function of neuronal cell membrane. Normal function of neuronal cell membrane requires appropriate composition of fatty in its structure. Present study was designed to compare the effect of short-term and long-term pretreatment with omega-3 fatty acids on scopolamine-induced amnesia and possible involvement of apoptotic or oxidative pathways. Male Wistar rats were gavaged by omega-3 fatty acids [60 mg/Kg [DHA + EPA]] or saline for 2 weeks [short-term model] or 8 weeks [Long-term model], then received intra-CA1 scopolamine [2 mg/rat]. Finally, the avoidance response was examined and hippocampus tissue was prepared. Intra-CA1 injection of scopolamine abolished the memory performance in rats. Short-term or long-term pretreatment with omega-3 fatty acids improved memory [p < 0.01 and p < 0.001, respectively]. Pretreatment for 2 weeks had no effect on the tissue Malondialdehyde [MDA] contents or SOD and CAT activity. In addition, pretreatment for 2 weeks with omega-3 fatty acids had no effects on tissue Bax and Bcl-2 expression. Conversely, long-term pretreatment with omega-3 fatty acids decreased tissue MDA contents [p < 0.01], SOD activity [p < 0.05] and increased CAT activity [p < 0.01]. Long-term pretreatment with omega-3 fatty acids also decreased Bax protein expression [p < 0.05] with no effect on the expression of Bcl-2 protein. In conclusion, long-term exposure to omega-3 fatty acids inhibited the scopolamine-induced oxidative stress, apoptosis and amnesia while the effect of short-term treatment was restricted to the improved memory without significant effect on apoptosis or oxidative stress. Therefore, long-term treatment with low doses of omega-3 fatty acids suggested a suitable treatment for amnesia

[ protective effect of azelaic acid 5% and minoxidil 5% combination therapy in reducing skin flap necrosis of rats]

One important limitation of random pattern skin flap in plastic surgery is the necrosis of distant parts of the flap resulting from ischemia. This effect cause unwanted increase in the costs and hospitalization. Previously, large number of factors has been evaluated to decrease the flap necrosis. In present study we used two drugs. Main reason was their mechanism of action that seems to be similar to preconditioning pathways. Fifty-six male rats were divided into four groups. In two groups 5% minoxidil or 5% azelaic acid were applied topically to the flap area before flap elevation. In some rats of minoxidil treated group, a non selective ATP sensitive potassium channel [KATP] blocker, glibenclamide [0.3mg/kg] was injected i.p. to evaluate the role of this channel in action. In azelaic acid treated rats, some were selected for evaluation of the role of nitric oxide and therefore L-NAME [20 mg/kg], a non-selective iNOS inhibitor, was administered. Seven days after operation, the extent of flap necrosis was calculated. Topical minoxidil or azelaic acid significantly recused necrotic area of skin flap to 42% [P<0.05] and 34% [P<0.01], respectively. Combination of minoxidil and azelaic acid was the most effictive intervantion on reducing of necrotic area to 26%. Glibenclamide abolished protective effect of minoxidil [P<0.001] and L-NAME inhibited the effect of azelaic acid on skin flap survival [P<0.05]. Both L-NAME and glibenclamide completely inhibited the effect of combination topical therapy. Present study suggested the role of KATP channels on minoxidil pathway and NO on L-NAME pathway of preserving skin flap survival. It seems that there is an overlap between the two pathways; however precise mechanism remained to be determined

[Assessment of cardiac troponin I in patients with pulmonary emboli and its relationship with right ventricular dysfunction]

Right ventricular dysfunction is common in major pulmonary embolisms. The purpose of this study was to evaluate the prevalence and diagnostic utility of cardiac troponin I and also to identify patients with RV dysfunction in pulmonary embolism. This study was conducted on 42 patients with pulmonary embolism in Ekbatan Hospital, in Hamedan city. Data from history, echocardiogram, and lung perfusion scan was obtained from medical records. Blood samples were obtained immediately after pulmonary embolism was diagnosed. Cardiac troponin was measured using chromatographic assay. Two patients [4.8%] had positive troponin I [>/= 0.5 microg/l], and 40 patients [95.2%] had negative troponin I [< 0.5 microg/l]. RV dysfunction was detected in 16 patients [38%]. RV dysfunction was detected in 1 of positive troponin I patients and 15 with negative troponin I [37.5%]. No significant relationship was found between RV dysfunction and troponin I level [p>0.05]. Our data demonstrates that troponin I measurement is not able to distinguish specifically between coronary and non- coronary causes of chest pain

mechanism of preventive effect of captopril on renal ischemia reperfusion injury is independent of ATP dependent potassium channels

Renal ischemia reperfusion [IR] injury has been a major source of concern during the past decades and angiotensin converting enzyme [ACE] inhibitors have been successfully used to prevent this injury. There have been some controversial reports about the involvement of KATP channels in the mechanism of action of ACE inhibitors. In this study, we examined the effect of KATP channel blocker [Glibenclamide] on preventive effect of captopril on renal IR injury. Male sprauge-dawley rats were pretreated with glibenclamide [1, 5 and 25 mg/kg] and/or captopril [5 mg/kg]. They were anesthetized using ketamine [50 mg/kg] and xylazine [10 mg/kg]. The left flank was incised and the left renal artery was clamped for 30 minutes. After that, the kidney was reperfused for 2 hours and then the animal was killed. The Right and left kidneys were removed and evaluated for microscopic damage. Captopril reduced renal IR injury while glibenclamide by itself caused no change. Glibenclamide did not change the preventive effect of captopril. It seems that the preventive effect of captopril is not directly mediated by KATP channels and further attention should be paid to other receptor-mediated angiotensin II effects