The Effect of Polygonum Multiflorum Extracts on Hematopoiesis and Platelet Production.

Abstract

To date, there is no ideal treatment for thrombocytopenia. We have proposed a possible mechanism of serotonin (5-HT) on megakaryocyte (MK) differentiation and platelet formation (Yang et al, Blood, 2003 suppl). The root of polygonum multiflorum thunb (Heshouwu) is an important ingredient of many commonly used prescriptions in Chinese medicine for promoting blood production. Polygonum multiflorum extracts (PME) also inhibit monoamine oxidase (MAO) and increase the level of 5-HT. Therefore, we hypothesize that polygonum multiflorum may have a promoting effect on thrombopoiesis via inhibition of monoamine oxidase (MAO) to increase 5-HT levels. The objective of this study was to investigate the hematopoietic role of PME in irradiated mice. PME (125 mg/kg/day) and TPO (12.5 ug/kg/day) were given by intra-peritoneal injection daily for 21 days starting from the day after irradiation (4 Gy). Peripheral blood platelets, white blood cells (WBC), and red blood cells (RBC) were analyzed from PME, TPO, and vehicle control groups on day 0, 7, 14 and 21. On day 21, the mice were sacrificed and bone marrow cells were harvested for CFU-MK, CFU-GM, BFU-E, CFU-GEMM and CFU-F (fibroblastoid) assays (n=8). We also investigated the in vitro effect of PME on CFU-F formation. Our results showed that PME enhanced the recovery of platelets, WBC, and RBC counts. Moreover, PME also promoted CFU-MK (30 ± 8 vs 15 ± 3 colonies/2 x 105 cells, p<0.01), CFU-GM (38 ± 7 vs 28 ± 7 colonies/2 x 105 cells, p<0.05), BFU-E (19 ± 3 vs 12 ± 4 colonies/2 x 105 cells, p<0.05), and CFU-F formation (36 ± 11 vs 23 ± 7 colonies/2 x 106 cells, p<0.01). Similar results were obtained in TPO-treated group. In in-vitro study, we further analyzed the effect of PME (0–500 ug/ml) on mouse CFU-F formation. The results showed that PME at 100–500 ug/ml significantly enhanced CFU-F formation (p<0.05, n=6). Our studies showed that PME enhances thrombopoiesis in vivo and the growth of bone marrow stromal cells in vitro. Therefore, we speculate that the thrombopoietic activity of PME may be mediated via promoting the bone marrow stromal cells. Although TPO has been effective as an agent for the recovery of platelet production after the onset of thrombocytopenia, long-term clinical usage of TPO may induce potential side effects such as thrombosis. Here we reported that the effect of PME is comparable with that of TPO on hematopoiesis and the production of platelets.