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黄花蒿中的莽草酸抑制糖尿病大鼠蛋白质糖基化。

Shikimic acid from Artemisia absinthium inhibits protein glycation in diabetic rats.

机构信息

Department of Biochemistry, Faculty of Science, Experimental Biochemistry Unit, King Fahd Medical Research Center, Bioactive Natural Products Research Group, King Abdulaziz University, Jeddah, Saudi Arabia.

出版信息

Int J Biol Macromol. 2019 Feb 1;122:1212-1216. doi: 10.1016/j.ijbiomac.2018.09.072. Epub 2018 Sep 15.

Abstract

This study investigated the impact of Shikimic Acid (SA) obtained from leaves of Artemisia absinthium on protein glycation in the retina of diabetic rats. The GC/MS analysis of A. absinthium showed that the most abundant bioactive compound was SA (CHO) with a measured retention Index (RI) of 1960 compared to that of the reference sample (1712). Male albino rats were divided into two main groups, Group I (control) and Group II (diabetic); Group II was further divided into four subgroups: Group IIa (diabetic control), Group IIb (diabetic rats were given SA orally [50 mg/kg, body weight (bw)/day], Group IIc diabetic rats were given SA orally [100 mg/kg, bw/day], and Group IId (diabetic rats were given metformin orally [100 mg/kg, bw/day] as positive control). The data obtained suggested that SA reduced glucose and glycated hemoglobin levels. In addition, SA also decreased the formation of glucose-derived advanced glycation end products. Interestingly, SA showed interference with the release of inflammatory mediators in retina and possess antioxidant potential. In conclusion, SA protected the tissues from detrimental effects of hyperglycemia and enhanced antioxidant activity. SA could be a potential lead in the process of drug development in the future to prevent retinopathy in diabetic subjects.

摘要

本研究探讨了从黄花蒿叶中提取的莽草酸(SA)对糖尿病大鼠视网膜蛋白糖基化的影响。GC/MS 分析表明,黄花蒿中含量最丰富的生物活性化合物是 SA(CHO),其保留指数(RI)为 1960,与参比样品(1712)相比。雄性白化大鼠分为两组,第一组(对照组)和第二组(糖尿病组);第二组进一步分为四个亚组:第二组 a(糖尿病对照组)、第二组 b(糖尿病大鼠口服 SA[50mg/kg,体重(bw)/天])、第二组 c(糖尿病大鼠口服 SA[100mg/kg,bw/day])和第二组 d(糖尿病大鼠口服二甲双胍[100mg/kg,bw/day]作为阳性对照)。结果表明,SA 降低了血糖和糖化血红蛋白水平。此外,SA 还减少了葡萄糖衍生的晚期糖基化终产物的形成。有趣的是,SA 对视网膜中炎症介质的释放表现出干扰作用,具有抗氧化潜力。总之,SA 保护组织免受高血糖的有害影响,并增强抗氧化活性。SA 可能成为未来开发药物预防糖尿病患者视网膜病变过程中的潜在先导化合物。

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