| Objective: Nutritional anemia is a curable disease, including iron deficiency anemia, megaloblastic anemia and mixed anemia, that is refer to hemoglobin biosynthesis or red blood cell (RBC) formation insufficient because of lacking of hematopoietic necessary nutrients. This disease still account for some proportion in benign hematonosis, and its pathogenesis may be related to cell apoptosis regulating besides low supplies of hematopoietic element lead to hemoglobin biosynthesis decrease or red blood cell (RBC) formation insufficient. Programmed cell death (PCD) or apoptosis is an autonomous process of cell death which has timing and spatial. As an important negative adjusting mechanism, apoptosis is related to embryo producing, tissue plasticity, hemopoiesis regulating, development and aging of human. B cell lymphoma/leukelmia-2(BCL-2) gene family is an important member of adjusting cell apoptosis gene families, and it has been proved by some studies that BCL-2 and BCL-associated X(BAX) genes of BCL-2 gene family and its products play an important role in the course and development process of nutritional anemia. The same as the BCL-2 and BAX genes, myeloid cell leukelmia-1(MCL-1) and BCL-2-homologous antagonist/killer (BAK) genes belong to BCL-2 gene family, and it has been discovered that they can adjust proliferation and apoptosis of a variety of solid tumors cells, but it is been not known the two genes are whether useful for nutritional anemia or not. The objective of this study is to detect the expression level of MCL-1 protein and BAK protein in serum of nutritional anemia patients and normal control people, analyze the clinical significance of the relationship between MCL-1 and BAK proteins and nutritional anemia development. Methods: 66 patients diagnosed for nutritional anemia at the hematology department of the Second Affiliated Hospital of Hebei Medical University for the time period March 2010 to December 2010 were selected for this study, they were divided into three groups: iron deficiency anemia group-29 cases, megaloblastic anemia group-15 cases and mixed anemia group-22 cases. All cases after diagnosed received 1 month treatment of hematopoietic nutrition elements.66 patients with nonnutritive anemia had 44 cases (iron-deficiency anemia group of 19 cases, megaloblastic anemia group of 10 cases, mixed anemia group of 15 cases) reviewed at post treatment. All nutritional anemia patients were diagnosed according to the"Blood disease diagnosis and curative standard"second edition, which is edited by Zhang Zhinan. 18 healthy people were randomly selected as normal control group.The patients before and after treatment were given the following detections: blood test (WBC, RBC, Hb, PLT, MCV, MVH, MCHC), reticulocyte count test (Ret), determinations of serum ferritin (SF), serum iron (Fe) , total iron binding capacity (TIBC), unsaturated iron binding capacity (UIBC), folate and vitamin B12(VB12), determinations of serum MCL-1 protein and BAK protein; the normal control group were given determinations of blood test, reticulocyte count, serum MCL-1 and BAK proteins. All this determinations were finished at our hospital laboratory. Serum MCL - 1 protein, BAK protein determinations were completed using enzyme-linked immune sorbent assay (ELISA).All the statistical analysis was dealt with SPSS13.0 software. The measurement data corresponding symmetric distribution were expressed as mean±standard deviation(SD),means of many different groups were compared by using one-way analysis of variance, means of two groups were compared by using S-N-K test, means of before and after treatment were compared by t-test, statistical correlation were done by Pearson analysis. P<0.05 had statistically significant difference.Results: 1 MCL-1, BAK proteins expression in normal control group: In normalcontrol group, the expression level of MCL-1 protein was (17.488±4.303)ug/L and BAK was (6.727±3.631)pg/ml.2 MCL-1, BAK proteins expression in nutritional anemia patients:Respectively, the expression level of MCL-1 protein in iron-deficiency anemia group, megaloblastic anemia group and mixed anemia group before treatment were (7.056±3.341)ug/L, (5.180±3.232)ug/L, (5.284±2.905)ug/L, compared with normal control group were significantly decreased, with statistically significant difference(P<0.001); BAK protein expression respectively were (9.843±3.541)pg/ml, (11.399±4.244)pg/ml, (9.194±4.173)pg/ml, compared with normal control group were significantly increased, with statistically significant difference(P<0.001). No statistical difference was seen between iron-deficiency anemia group, megaloblastic anemia group and mixed anemia group post treatment and control group (P>0.05).3 MCL-1, BAK proteins expression in each group of nutritional anemia patients: The expression level of MCL-1, BAK proteins in each group of nutritional anemia patients before treatment didn't have statistical difference (P>0.05); MCL-1, BAK proteins expression didn't have statistical difference in each group of nutritional anemia patients post treatment (P>0.05). The expression level of MCL-1 protein in mild anemia group, moderate anemia group, severe anemia group of nutritional anemia patients before treatment respectively were (9.924±1.991)ug/L, (5.354±1.713)ug/L, (2.136±0.950)ug/L, and the difference were significant, with statistical difference (P<0.05); BAK protein expression respectively were (5.739±2.518)pg/ml, (10.337±2.237)pg/ml, (14.267±1.849) pg/ml, the difference also had statistical difference (P<0.05). In hemoglobin normal group and hemoglobin abnormal group of nutritional anemia patients post treatment, MCL-1 protein expression respectively were (15.325±4.136)ug/L, (12.500±3.848)ug/L, with statistical difference (P<0.05); the expression level of BAK protein respectively were (5.023±2.096)pg/ml, (7.964±2.200)pg/ml, with statistical difference (P <0.05). 4 MCL-1, BAK proteins expression in nutritional anemia patients before and post treatment: In iron-deficiency anemia patients group before and post treatment, MCL-1 protein expression respectively were (7.056±3.341)ug/L, (14.506±4.337)ug/L, BAK protein were (9.843±3.541)pg/ml, (5.771±2.521)pg/ml, the difference had statistical difference (P<0.05); In megaloblastic anemia patients group before and post treatment, the expression level of MCL-1 protein respectively were (5.180±3.232)ug/L, (14.457±4.605)ug/L, BAK protein were (11.399±4.244)pg/ml, (4.966±2.122)pg/ml, with statistical difference (P<0.05); In mixed anemia patients group before and post treatment, MCL-1 protein expression respectively were (5.284±2.905)ug/L, (14.491±4.474)ug/L, BAK protein were (9.194±4.173)pg/ml, (5.972±2.390)pg/ml, the difference also had statistical difference (P<0.05).5 The relationship between expression of MCL-1 and BAK: The Pearson correlation analysis was done for the relationship of MCL-1, BAK proteins in nutritional anemia patients, the result was that there was a negative correlation between MCL-1 and BAK with the standard P<0.05, r=-0.858, the linear regression equation was Y=13.384-0.751X.Conclusion:1 Apoptosis adjustment factors involve the process both onset and recovery of nutritional anemia, which prove besides lacking of nutrition elements relatively or absolutely, there is some relationship between apoptosis adjustment disorder and nutritional anemia.2 The nutrition elements in short supply causes apoptosis adjustment disorder, MCL-1protein expression changes to lower level, BAK changes to higher, cell apoptosis increase. After the lacking of nutrition elements is corrected, the two proteins expression can come to normal level, that suggest the foundation can supply a new proof for nutritional anemia diagnosis, according the expression of MCL-1, BAK proteins can judge prognosis. The difference of nutrition elements lacking don't impact MCL-1, BAK proteins expression. 3 MCL-1, BAK proteins have mutual antagonism role for nutritional anemia patients, the two proteins adjust cell apoptosis together. |
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