BACKGROUND: Sickle cell anemia (SCA) is a hereditary chronic hemolytic anemia with several clinical consequences. Intravascular sickling of red blood cells leads to multi-organ dysfunction. Moreover, several biochemical abnormalities have been associated with SCA. Gum arabic (GA) is an edible dried gummy exudate obtained from Acacia Senegal tree. GA showed antioxidant and cytoprotective activities and demonstrated protection against hepatic, renal, and cardiac toxicities in experimental rats. We hypothesized that regular intake of GA improves renal and liver functions in patients with SCA. METHODS: Forty-seven patients (5–42 yr) carrying hemoglobin SS were recruited. The patients received 30 g/day GA for 12 weeks. Blood samples were collected before administering GA and then after 4, 8, and 12 weeks. Liver enzymes, total protein, albumin, electrolytes, urea, creatinine, and uric acid were determined in the serum. The study was approved by the Al Neelain University Institutional Review Board and Research Ethics Committee Ministry of Health. The trial was registered at ClinicalTrials.gov (identifier: NCT02467257). RESULTS: GA significantly decreased direct bilirubin level [statistical significance (P-value)=0.04]. It also significantly decreased serum alanine transaminase level after 4 weeks, which was sustained till the 8th week. GA, however, had no effect on serum aspartate transaminase level. In terms of renal function, GA decreased serum urea level but the effect was not sustained after the first month. CONCLUSION: GA may alter the disease severity in SCA as demonstrated by its ability to decrease direct bilirubin and urea levels in the serum.
Acacia ; Alanine Transaminase ; Anemia, Hemolytic ; Anemia, Sickle Cell ; Animals ; Aspartate Aminotransferases ; Bilirubin ; Cardiotoxicity ; Creatinine ; Electrolytes ; Erythrocytes ; Ethics Committees, Research ; Exudates and Transudates ; Gingiva ; Gum Arabic ; Hemoglobin, Sickle ; Humans ; Liver ; Rats ; Senegal ; Trees ; Urea ; Uric Acid

BACKGROUND: Although AT1 receptor antagonist can protect myocardium against ischemia/reperfusion injury at the cellular level, the in vivo effect and the mechanisms of this effect have not yet been characterized. The present study was designed to examine the myocardial protective effect of irbesartan(an AT1 receptor antagonist) in ischemia-reperfusion model of rats, and to elucidate the role of apoptosis as a biological mechanism mediating reperfusion injury. MATERIAL AND METHOD: An inert vehicle(10% gum arabic: group I, n=14) or irbesartan(50mg/kg/day: group II, n=12) was administered to Sprague-Dawley rats orally every 24 hours for 3 days. Animals were subjected to a 45-minute left coronary artery ligation followed by a 2-hour reperfusion, then the hearts were harvested. The ratio of myocardial infarct area/ischemic risk area was assessed through TTC(triphenyltetrazolium chloride) staining. Degree of apoptosis was evaluated by analyzing the DNA fragmentation attern on agarose gel electrophoresis and TUNEL(TdT-mediated dUDP nick end labeling) staining. Western blot analysis was performed to estimate the expression of the proteins known to regulate apoptosis such as Bcl-2(B-cell lymphoma 2 gene) and Bad, and the MAPKs(mitogen-activated protein kinases) implicated in signal transduction such as ERK (extracellular signal-regulated kinase) and p-38. RESULT: The ratio of infarct area/ischemic area at risk in group II was significantly smaller than that of group I(42.6+/-2.7% vs. 64.1+/-4.6% ; p<0.005). Agarose gel electrophoresis revealed discrete DNA laddering in the ischemic zone of group I, but DNA ladder formation was attenuated in group II. The expressions of Bcl-2 and ERK1 were higher in ischemic area of group II compared to that of group I. CONCLUSION: AT1 receptor antagonist, irbesartan, was effective in reducing myocardial reperfusion injury in vivo. This effect can be attributed partially to the attenuation of cardiomyocyte apoptosis, which was suggested by the increased expression of Bcl-2.
Angiotensin II ; Angiotensins* ; Animals ; Apoptosis ; Blotting, Western ; Cell Death ; Coronary Vessels ; DNA ; DNA Fragmentation ; Electrophoresis, Agar Gel ; Gum Arabic ; Heart ; Ligation ; Lymphoma ; Myocardial Infarction ; Myocardial Reperfusion Injury ; Myocardium ; Myocytes, Cardiac ; Negotiating ; Rats* ; Rats, Sprague-Dawley ; Receptor, Angiotensin, Type 1* ; Reperfusion Injury* ; Reperfusion* ; Signal Transduction