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首页> 外文期刊>Life sciences >Troglitazone can prevent development of type 1 diabetes induced by multiple low-dose streptozotocin in mice.
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Troglitazone can prevent development of type 1 diabetes induced by multiple low-dose streptozotocin in mice.

机译：曲格列酮可预防小鼠多种低剂量链脲佐菌素诱导的1型糖尿病的发展。

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Recent investigations suggest that cytotoxic cytokines such as tumor necrosis factor (TNF)alpha and interleukin (IL)-1beta or free radicals play an essential role in destruction of pancreatic beta cells in Type 1 diabetes and that, therefore, anti-oxidant or anti-TNF alpha and IL-1beta therapy could prevent the development of Type I diabetes. Troglitazone belongs to a novel class of antidiabetic agent possessing the ability to enhance insulin action provably through activating PPAR gamma and to scavenge free radicals. In the present study, we examined whether troglitazone can prevent the development of Type 1 diabetes in multiple, low-dose streptozotocin (MLDSTZ)-injected mice. In addition, effects of troglitazone on cytokine-induced pancreatic beta cell damage were examined in vitro. Type 1 diabetes was induced by MLDSTZ injection to DBA/2 mice (40 mg/kg/day for 5 days). Troglitazone was administered as a 0.2% food admixture (240 mg/kg/day) for 4 weeks from the start of or immediately after STZ injection. MLDSTZ injection elevated plasma glucose to 615 +/- 8 mg/dl 4 weeks after final STZ injection and was accompanied by infiltration of leukocytes to pancreatic islets (insulitis). Troglitazone treatment with MLDSTZ injection prevented hyperglycemia (230 +/- 30 mg/dl) and, suppressed insulitis and TNF alpha production from intraperitoneal exudate cells. TNF alpha (10 pg/ml) and IL-1beta (1 pg/ml) addition to hamster insulinoma cell line HIT-T15 for 7 days in vitro decreased insulin secretion and cell viability. Simultaneous troglitazone addition (0.03 to approximately 3 microM) significantly improved cytokine-induced decrease in insulin secretion and in cell viability. These findings suggest that troglitazone prevents the development of Type 1 diabetes in the MLDSTZ model by suppressing insulitis associated with decreasing TNF alpha production from intraperitoneal exudate cells and the subsequent TNF alpha and IL-1beta-induced beta cell damage.
机译：最近的研究表明，细胞毒性细胞因子，例如肿瘤坏死因子（TNF）α和白介素（IL）-1beta或自由基在1型糖尿病的胰腺β细胞破坏中起着至关重要的作用，因此，抗氧化剂或抗氧化剂TNFα和IL-1beta治疗可预防I型糖尿病的发展。曲格列酮属于一类新型的抗糖尿病药，具有通过激活PPARγ来证明可增强胰岛素作用并清除自由基的能力。在本研究中，我们检查了曲格列酮是否可以预防多次低剂量链脲佐菌素（MLDSTZ）注射的小鼠中1型糖尿病的发展。另外，在体外检查了曲格列酮对细胞因子诱导的胰腺β细胞损伤的作用。通过向DBA / 2小鼠MLDSTZ注射（40毫克/千克/天，持续5天）诱导1型糖尿病。从开始注射STZ或注射STZ之后的4周，将曲格列酮以0.2％的食品添加剂（240 mg / kg /天）的剂量给药。最终STZ注射后4周，MLDSTZ注射将血浆葡萄糖升高至615 +/- 8 mg / dl，并伴有白细胞浸入胰岛（胰岛炎）。曲格列酮注射MLDSTZ可以预防高血糖症（230 +/- 30 mg / dl），并且可以抑制腹膜内渗出液引起的胰岛炎和TNFα的产生。在体外向仓鼠胰岛素瘤细胞系HIT-T15添加TNF alpha（10 pg / ml）和IL-1beta（1 pg / ml）会降低胰岛素分泌和细胞活力。曲格列酮的同时添加（0.03至约3 microM）显着改善了细胞因子诱导的胰岛素分泌和细胞活力的降低。这些发现表明曲格列酮通过抑制与腹膜内渗出液中TNFα产生减少以及随后的TNF alpha和IL-1beta诱导的beta细胞损伤相关的胰岛素样炎，从而预防了MLDSTZ模型中1型糖尿病的发生。

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