Derangement of hemopoiesis and hematological indices in Khat (Catha edulis) - treated rats

The purpose of this study was to identify the sub-acute toxic effects of Khat (Catha edulis) on hemopoiesis and hematological indices of white albino rats. Two groups, each of 10 rats, were used. In the experimental group, a hydro-ethanol extract of C. edulis was administered orally to rats, daily, in single doses of 500 mg/kg body weight, for for weeks. The control group received equivalent amounts of normal saline. Our results show, for the first time, that oral administration of C. edulis hydro-ethanol extract caused significant derangement in hemopoiesis and in gross hematological indices in rats, characterized by macrocytic anemia and leucopenia. Our data show statistically significant decreases in total leukocytes count (TLC) in which, hemoglobin concentration (Hb. conc.), packed cell volume (PCV), and red cell count (RCC), accompanied by significant increases in mean cell volume (MCV), red blood cell distribution width (RDW) and platelets count with no change in mean hemoglobin concentration (MHC). In peripheral blood smears (PBS) of treated rats, there were evidences of dyserythropoiesis- impaired hemoglobinization, macrocytosis, poikilocytosis and anisocytosis, and dysgranulopoiesis- giant forms, hypersegmented neutrophils and bizarre nuclear shapes. In conclusion, our results indicate that oral administration of a hydro-ethanol extract of C. edulis adversely affected blood cell formation and induced macrocytic anemia and leukopenia in rats. However, the exact mechanisms of these hematological changes produced by Khat are still in need for further studies.Keywords:Catha edulis, hemopoiesis, anemia, leukopenia, ratsAfrican Journal of Biotechnology, Vol. 13(2), pp. 349-355, 8 January, 201

Thrombocytopenia in Patients With Chronic Hepatitis C: A Possible Role of HCV on Platelet Progenitor Cell Maturation

A total of 30 patients with chronic hepatitis C (HCV) thrombocytopenia (TP) and 20 healthy controls were studied. Both groups were subjected to complete medical history, clinical examination in addition to assessment of hepatitis markers: level of thrombopoietin (Tpo), Geimsa-stained bone marrow smears, and in vitro short-term megakaryocytic progenitors culture (CFU-MK). Serum Tpo level was significantly elevated in patients with TP HCV. Short-term CFU-MK showed an evident depression in the colony-forming unit-megakaryocyte (CFU-meg). There is a positive correlation between the number of CFU-meg and the platelet count and between serum Tpo level and prothrombin time, transaminase, albumin, and the Child Pugh score of liver disease; a negative correlation between serum Tpo level and the number of CFU-meg and between serum Tpo level and the platelet count. Thus, the level of Tpo could be an indicator of intact functional response of the hepatocytes

Metformin Protects against Diabetic Cardiomyopathy: An Association between Desmin–Sarcomere Injury and the iNOS/mTOR/TIMP-1 Fibrosis Axis

The intermediate filament protein desmin is essential for maintaining the structural integrity of sarcomeres, the fundamental unit of cardiac muscle. Diabetes mellitus (DM) can cause desmin to become dysregulated, following episodes of nitrosative stress, through the activation of the iNOS/mTOR/TIMP-1 pathway, thereby stimulating collagen deposition in the myocardium. In this study, type 2 diabetes mellitus (T2DM) was induced in rats. One group of animals was pre-treated with metformin (200 mg/kg) prior to diabetes induction and subsequently kept on metformin until sacrifice at week 12. Cardiac injuries developed in the diabetic rats as demonstrated by a significant (p p < 0.0001) correlation between desmin tissue levels/sarcomere damage and glycated hemoglobin, heart rate, iNOS, mTOR, and fibrosis was observed. These findings demonstrate an association between damage of the cardiac contractile unit—desmin and sarcomere—and the iNOS/mTOR/TIMP-1/collagen axis of fibrosis in T2DM-induced cardiomyopathy, with metformin exhibiting beneficial cardiovascular pleiotropic effects