ABSTRACT
Objective: Commiphora gileadensis is a small tree under the genus Commiphora. Previous studies showed medical applications, such as antibacterial and antihypertensive, for C. gileadensis. Methods: Sixty naïve mice were classified into six groups: control, C. gileadensis sap-treated group, C. gileadensis methanol extract-treated group, C. gileadensis acetone extract-treated group, heparin-treated group, and aspirin-treated group. Blood samples from each mouse in the six groups were collected in EDTA, sodium citrate, and heparin tubes. The body weight of each mouse was measured at the beginning and end of the experiment. Furthermore, complete blood count, kidney and renal function tests, coagulation profiles, prothrombin time (PT), activated partial thromboplastin time (aPTT), international normalized ratio (INR), D-dimer, and fibrinogen concentrations were estimated for each mouse. Results: The sodium, potassium, chloride, blood urea nitrogen, creatinine, alanine transaminase, and aspartate transaminase levels did not show statistical differences between all groups. Moreover, PT, aPTT, and INR were prolonged in the C. gileadensis sap, methanol, and acetone extracts-treated mice compared with those in the heparin and aspirin-treated groups (P < 0.01). D-dimer and fibrinogen concentrations did not show significant statistical differences between all groups. Conclusion: The current study concludes that the C. gileadensis sap, methanol, and acetone extracts prolonged PT, aPTT, and bleeding time in naïve mice more than heparin and aspirin. This means that the C. gileadensis extracts may have antithrombotic activity and may be used in the future to resolve intravascular thrombosis in patients having prosthetic valves.
ABSTRACT
Microcystin Leucine-Arginine (MC-LR) is a toxin produced by the cyanobacteria Microcystis aeruginosa. It is the most encountered and toxic type of cyanotoxins. Oxidative stress was shown to play a role in the pathogenesis of microcystin LR by the induction of intracellular reactive oxygen species (ROS) formation that oxidize and damage cellular macromolecules. In the present study we examined the effect of acute MC-LR dose on the cardiac muscle of BALB/c mice. Afterwards, melatonin and N-acetyl cysteine (NAC) were assayed and evaluated as potential protective and antioxidant agents against damages generated by MC-LR. For this purpose, thirty mice were assigned into six groups of five mice each. The effect of MC-LR was first compared to the control group supplied with distilled water, then compared to the other groups supplied with melatonin and NAC. The experiment lasted 10 days after which animals were euthanized. Biomarkers of toxicity such as alkaline phosphatase activity, lipid peroxidation, protein carbonyl content, reduced glutathione content, serum lactate dehydrogenase and serum sorbitol dehydrogenase were assayed. Results showed that toxin treated mice have experienced significant oxidative damage in their myocardial tissue as revealed by noticeable levels of oxidative stress biomarkers and by the reduction in alkaline phosphatase activity. Whereas, melatonin and NAC treated mice manifested lesser oxidative damages. Our findings suggest a potential therapeutic use of melatonin and N-acetyl cysteine as antioxidant protective agents against oxidative damage induced by MC-LR.
