壳寡糖促胰岛细胞增殖、胰岛素分泌及调节餐后血糖作用的研究

目的研究酶解法制备的壳寡糖对原代培养的胰岛细胞和胰岛β细胞系NIT-1的促增殖及胰岛素分泌作用,探讨在体内壳寡糖降低链脲佐菌素诱导的糖尿病大鼠的餐后2 h血糖的作用。方法通过壳聚糖酶降解壳聚糖制备得到水溶性、低分子量的壳寡糖,在细胞水平上,通过形态学观察、MTT比色法、放射免疫等方法研究不同浓度的壳寡糖对于原代培养的大鼠胰岛细胞和胰岛β细胞系NIT-1细胞的增殖及促胰岛素分泌作用;体内实验,通过一般状态观察、餐后2 h血糖、尿糖、糖耐量测定研究了壳寡糖对链脲佐菌素诱导的糖尿病大鼠降低餐后2 h血糖和改善葡萄糖耐量的作用。结果壳寡糖对于原代培养的大鼠胰岛细胞和胰岛β细胞体外增殖具有明显的促进作用并可以显著促进原代培养胰岛细胞的胰岛素分泌。不同剂量的壳寡糖均能不同程度改善糖尿病大鼠的体重减轻、多饮、多食等症状,降低餐后2 h血糖值和尿糖,改善葡萄糖耐量。结论壳寡糖有多种不同的生物等功能,尤其在糖尿病的治疗方面有潜在的应用价值。

DEPLETION OF O^6-METHYLGUANINE-DNA METHYLTRANSFERASE ACTIVITY AND POTENTIATION OF 1-(4-AMINO-2-METHYL-5- PYRIMIDINYL) METHYL-3 (2-CHLOROETHYL)-3-NITRO- SOUREA ANTITUMOR EFFECT BY STREPTOZOTOCIN

O6-methylguanine-DNA Methyltransferase (MGMT) can specifically repair the DNA demage Induced by chioroethylnitrosoureas (CENU) such at 1-(4-amino-2-methyt-pyrlmidinyl) methyl-3-(2-chloroethyl-)-3-nitrosourea (ACNU), constituting the molecular basis of tumor cell resistance to CENU. The present study demonstrated that sensitization of resistant tumor cells to ACNU could be achieved by streptozotocin (STZ) treatment which could deplete MGMT activity in vitro and in vivo. It suggested that depletion of the molecular basis of tumor cell resistance to chemotherapeutic agents might be a practicable way to improve the effectiveness of tumor chemotherapy.