Yanjie He1, Tianhan Kong, Weihua Dong. 1. Department of Pathophysiology, Guangzhou Medical College, Guangzhou, Guangdong 510182, China.
Abstract
OBJECTIVE: To study the effects of Scorpion venom polypeptide (SVP) on the irradiated hematopoietic progenitor cells and the initial research of its mechanism. METHODS AND MATERIALS: (1) MTT array was used to select the effective concentration of SVP that had proliferate action on the irradiated early hematopoietic cells (K562), just like the doses of experiment in vitro; (2) The male BALB/c mice were divided into NS control group, SVP IV group and SVP V group. After treatment and sublethal irradiation, the C-KIT and IL-6Ralpha levels of bone marrow cells were detected by immunohistochemistry and tissue array; (3) The bone marrow cells of the normal BALB/c mice, given to SVP IV and SVP V after different action times respectively, were taken to extract the total proteins inside the cell, the phosphorylated STAT3 protein levels in JAK-STAT signal transduction pathway were detected by Western blot array. RESULTS: (1) 30mg/L SVP IV has an obvious effect to accelerate K562 cell proliferation; (2) The C-KIT and IL-6Ralpha expression on bone marrow cell surfaces in SVP IV and SVP V groups were negative (control with the saline group, p>0.05); (3) The phosphorylated STAT3 protein levels in bone marrow cells of SVP IV group had a rise-and-fall trend within 30min, while the test of SVP V group showed that the phosphorylated STAT3 protein levels obviously elevated after 30min. CONCLUSIONS: The results show that certain SVP IV concentration can protect the hematopoietic progenitor cells after irradiation, and the underlying mechanism of SVP accelerating the hematopoietic recovery in irradiated mice may be related to the activation of the JAK-STAT signal pathway.
OBJECTIVE: To study the effects of Scorpion venom polypeptide (SVP) on the irradiated hematopoietic progenitor cells and the initial research of its mechanism. METHODS AND MATERIALS: (1) MTT array was used to select the effective concentration of SVP that had proliferate action on the irradiated early hematopoietic cells (K562), just like the doses of experiment in vitro; (2) The male BALB/c mice were divided into NS control group, SVP IV group and SVP V group. After treatment and sublethal irradiation, the C-KIT and IL-6Ralpha levels of bone marrow cells were detected by immunohistochemistry and tissue array; (3) The bone marrow cells of the normal BALB/c mice, given to SVP IV and SVP V after different action times respectively, were taken to extract the total proteins inside the cell, the phosphorylated STAT3 protein levels in JAK-STAT signal transduction pathway were detected by Western blot array. RESULTS: (1) 30mg/L SVP IV has an obvious effect to accelerate K562 cell proliferation; (2) The C-KIT and IL-6Ralpha expression on bone marrow cell surfaces in SVP IV and SVP V groups were negative (control with the saline group, p>0.05); (3) The phosphorylated STAT3 protein levels in bone marrow cells of SVP IV group had a rise-and-fall trend within 30min, while the test of SVP V group showed that the phosphorylated STAT3 protein levels obviously elevated after 30min. CONCLUSIONS: The results show that certain SVP IV concentration can protect the hematopoietic progenitor cells after irradiation, and the underlying mechanism of SVP accelerating the hematopoietic recovery in irradiated mice may be related to the activation of the JAK-STAT signal pathway.