葡萄糖胺调节膜和细胞离子稳态:加速衰老和自然衰老大鼠的研究

Komal Saraswat, Raushan Kumar, S. Rizvi
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引用次数: 0

摘要

氨基葡萄糖是一种氨基多糖,已被广泛用于缓解骨关节炎。在本研究中,研究人员试图评估葡萄糖胺(一种热量限制模拟物)在d -半乳糖(D-gal)诱导的大鼠加速衰老和自然衰老模型中对红细胞膜转运体的潜在保护作用,特别是Ca2+- atp酶(PMCA泵)、Na+/K+- atp酶(NKA泵)、Na+/H+交换剂(NHE)和氧化还原生物标志物。该研究包括年幼(3-4个月大;150±20 g)自然陈酿(24个月以上;420±20 g)和d -半乳糖诱导龄(3-4月龄;150±20 g,与D-Gal按300 mg/kg b.w.皮下注射)Wistar雄性白化大鼠。所有大鼠均添加盐酸氨基葡萄糖(300 mg/kg体重)12周。D-Gal和自然老龄大鼠Ca2+- atp酶活性、Na+/K+- atp酶活性和诱导的NHE活性均显著(P < 0.05)降低。细胞内Ca2+离子、蛋白羰基和脂质氢过氧化物等氧化还原生物标志物水平也显著升高(P < 0.05)。这些结果在补充葡萄糖胺的大鼠中被发现是相反的。我们的研究结果表明,葡萄糖胺的补充通过保护红细胞膜转运蛋白免受年龄相关的改变来改善离子稳态。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Glucosamine modulates membrane and cellular ionic homeostasis: studies on accelerated senescent and naturally aged rats
ABSTRACT Glucosamine, an amino-polysaccharide, has been widely used for alleviating osteoarthritis. . In the present study, attempts have been made to evaluate the potential role of glucosamine, a caloric restriction mimetic (CRM), for erythrocyte membrane transporter protection in D-galactose (D-gal) induced accelerated and natural aging models of rat specifically Ca2+-ATPases (PMCA pump), Na+/K+-ATPases (NKA pump), and the Na+/H+ exchanger (NHE) and redox biomarkers during aging. The study comprised of young (3–4 months old; 150 ± 20 g), naturally aged (above 24 months; 420 ± 20 g) and D-galactose-induced aged (3–4 months old; 150 ± 20 g, administered with D-Gal at 300 mg/kg B.W., subcutaneously) male albino rats of Wistar strain. All the rats were supplemented with Glucosamine hydrochloride (300 mg/kg body weight) for 12 weeks. There was a significant (P < 0.05) decrease in the activity of Ca2+-ATPases, Na+/K+-ATPases and induced NHE activity in D-Gal and naturally old rats. Levels of redox biomarkers such as intracellular Ca2+ ion, protein carbonyl, and lipid hydroperoxides were also found to be increased significantly (P < 0.05). These results were found to be reversed in the rats supplemented with glucosamine. Our findings suggest that glucosamine supplementation improves ion homeostasis by protecting the erythrocyte membrane transporters against age-related alterations.
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