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首页> 外文期刊>Life sciences >Low proliferation capacity of lymphocytes from alloxan-diabetic rats: involvement of high glucose and tyrosine phosphorylation of Shc and IRS-1.
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Low proliferation capacity of lymphocytes from alloxan-diabetic rats: involvement of high glucose and tyrosine phosphorylation of Shc and IRS-1.

机译：四氧嘧啶糖尿病大鼠淋巴细胞的低增殖能力：Shc和IRS-1的高葡萄糖和酪氨酸磷酸化的参与。

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摘要

The proliferation capacity of lymphocytes obtained from mesenteric lymph nodes of control and alloxan-diabetic (40 mg/kg) rats in response to concanavalin A (ConA) and lipopolysaccharide (LPS) stimuli was examined. Proliferation response of lymphocytes from diabetic rats was significantly reduced under Con A (43%) and LPS (46%) stimulation as compared with the control group. Insulin (166 microM) promoted a marked increase of lymphocyte proliferation (7.5-fold) in the control group and this response was much lower (2.6-fold) in lymphocyte from diabetic rats. Cells were also cultured in medium containing glucose at 5, 10 or 20 mM. High glucose concentration (20 mM) caused a marked inhibition of lymphocyte proliferation reaching the values of the diabetic group. In lymphocytes from control rats, the degree of Shc tyrosine phosphorylation was gradually increased, whereas that of cells from diabetic rats was much lower in response to insulin. In lymphocytes obtained from control rats, the tyrosine phosphorylation of IRS-1 was time-dependent on insulin. In cells from diabetic rats, the basal tyrosine phosphorylation of IRS-1 was higher than that of control rats, however, there was no further phosphorylation after insulin addition. We conclude that the response of lymphocyte proliferation from diabetic rats to Con A and LPS stimuli is decreased but insulin was able to promote a significant proliferative effect on these cells. Also, high glycemia in addition to the lack of insulin participates in the reduced proliferation capacity of lymphocytes from diabetic rats.
机译：检查了从对照和四氧嘧啶糖尿病大鼠（40 mg / kg）的肠系膜淋巴结中获得的淋巴细胞对伴刀豆球蛋白A（ConA）和脂多糖（LPS）刺激的增殖能力。与对照组相比，在Con A（43％）和LPS（46％）刺激下，糖尿病大鼠淋巴细胞的增殖反应显着降低。在对照组中，胰岛素（166 microM）促进了淋巴细胞增殖的显着增加（7.5倍），而糖尿病大鼠淋巴细胞的这种反应则低得多（2.6倍）。还在含有5、10或20mM葡萄糖的培养基中培养细胞。高葡萄糖浓度（20 mM）导致淋巴细胞增殖达到糖尿病组的值受到明显抑制。在对照大鼠的淋巴细胞中，Shc酪氨酸磷酸化程度逐渐增加，而糖尿病大鼠的细胞对胰岛素的反应程度则低得多。在从对照大鼠获得的淋巴细胞中，IRS-1的酪氨酸磷酸化时间依赖于胰岛素。在糖尿病大鼠的细胞中，IRS-1的基础酪氨酸磷酸化高于对照大鼠，但是在添加胰岛素后不再有磷酸化。我们得出的结论是，糖尿病大鼠淋巴细胞对Con A和LPS刺激的淋巴细胞增殖反应有所降低，但胰岛素能够促进这些细胞的明显增殖作用。此外，除了缺乏胰岛素外，高血糖症还参与了糖尿病大鼠淋巴细胞增殖能力的降低。

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