| Growth hormone (GH) is one kind of protein hormone, which is secreted by eosinophilic granulocyte of anterior pituitary. Its effect at the level of physiological dose is to promote children's normal growth development. During adult stage, its secretion is decreased. However it is very important to maintain normal human component. At the level of pharmacological dose, its function is to construct metabolism including improving glucose oxidation to increase energy lever, to accelerate lipodieresis and glyconeogenesis, and to enhance protein synthesis. In 1985, recombinant human growth honnone(rhGH) was successfully synthesized, and was formally allowed to be used in clinical practice, which made a good curativeeffect on improving nutrition condition, improving nitrogen balance, and wound healing in high catabolic patients. Several studies have shown that nutritional support of GH intervention increases whole-body and skeletal muscle protein synthesis and improves patients' nutritional condition significantly. However, some studies suggest that GH and/or its mediator, IGF-1, are cellular mitogen and may support tumor growth. It is possible that the potential salutary effects of GH may be offset by a tumor-promoting effect. Several animal studies on solid carcinoma indicate that GH administered to experimental tumor-bearing animal did not stimulate tumor growth. Cell cycle kinetics analysis showed that GH could increase the percentage of S-phase cell. However, there is no report for using GH to promote the sensitivity of cycle specific medicine to tumor. In this study, the model of proventriculus squamous carcinoma hgepatic metastases in mice was made and animals were treated with rhGH and flurouracil (5-FU). Body weight, liver weight, the number of liver metastases, lifespan and cell cycle kinetics were observed to evaluate GH's effects on the growth of tumor and on the effects of GH combining with 5-FU in the tumor-bearing mice.Methods: A transplantable cell line of proventriculussquamous cell carcinoma in the mice (MFC) was used m this study. Cell was harvested in logarithmic growth period, digested with 0.25% trysin, counted and regulated the concentration about IxlO7 cells/ml. Cell viability was determined by the trypan blue exclusion method. This study is consisted of two sections:1. Sixteen healthy 615 inbreed mice were anesthetized intraperitoneally with 2% pentobarbreal sodium, and then surgical procedure was taken in abdominal to expose spleen. 0.2ml single cell suspensions were injected into spleen to make liver metastases model, 75% alcohol-cotton was used to hemostasis by compression and 95% alcohol-cotton was used to kill cancer cell, then abdominal wall were sutured. After surgery, 2-3 mice were sacrificed every week, and the others were used to observe the survival time. The liver metastases condition were dissected and recorded for all animals.2. Forty-eight 615 inbreed mouse which weighted 18-23g were randomly allocated into 4 groups: control (NS); growth hormone (GH); fluorouracil (5-FU); and GH plus 5-FU (GH/5-FU). There were 12 animals in each group. MFC single cell suspension was injected into the spleen in the way described before. After 15 days of surgery, rhGH was injected subcutaneously (s.c.) at a dosage of2IU/kg body weight GH group daily; 5-FU was injected intraperitoneally (i.p.) at a dosage of 20 mg/kg body weight for 5-Fu group daily; rhGH 211/kg body weight and 5-FU 20 mg/kg body weight were injected s.c. and i.p. respectively for GH/5-FU group; of normal saline were injected s.c. and i.p. respectively at the same amount for NS group. The animals' body weights were measured every week. On day 28 after surgery, all animals were sacrificed. The number of liver metastases and weight of liver were measured and tumor was biopsied for cell cycle analysis by flow cytometry (FCM). Furthermore, thirty-two mice were randomly divided into four groups and were injected with MFC cells, rhGH, 5-FU at the same dosage and same time as the 48 mice d...
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