ABSTRACT
Ischemia reperfusion injury [IR injury] is a common problem in clinical conditions. Researches have frequently revealed that ATP- sensitive potassium [K[ATP]] channels and nitric oxide plays a role in protection against ischemic injury in skeletal muscle. The present study aimed at evaluating the possible link between this two pathways. Sixty-eight male wistar rats, were pretreated with saline, diazoxide [K[ATP] opener; 45 mg/Kg, IP], glibenclamide [K[ATP] inhibitor; 5 mg/Kg], or L-NAME [iNOS inhibitor; 20 mg/Kg, IP] before 3 h ischemia and 2 h reperfusion. Activities of antioxidant enzymes superoxide dismutase [SOD] and catalase [CAT], and the level of malondialdehyde [MDA] and expression of iNOS were measured in muscle tissue. Tissue MDA content was significantly increased by IR [p < 0.001]. Diazoxide significantly decreased the IR-induced elevation of tissue MDA level [p < 0.05] and Glibenclamide increased MDA [p < 0.05 vs. IR group]. L-NAME inhibited the effect of diazoxide on decreasing MDA [p < 0.01 vs., diazoxide+IR group] and IR decreased the activity of SOD and CAT [p < 0.01], while pretreatment with diazoxide increased activity of SOD and CAT [p < 0.01]. Glibenclamide decreased SOD and CAT activity after IR [p < 0.05]. L-NAME pretreatment in diazoxide-treated rats abolished the effect of diazoxide on increasing the activity of SOD and CAT [p < 0.05 vs. Diaz+IR]. Expression of iNOS was increased by IR [p < 0.01 vs. Sham group]. Diazoxide significantly decreased iNOS expression after IR [p < 0.05 vs. IR]. L-NAME significantly decreased iNOS expression after IR [p < 0.01] in diazoxide-treated rats [p < 0.01 vs. Diaz+IR]
ABSTRACT
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