School of Nursing, Army Medical University, Chongqing, PR China.
Key Lab of Birth Defects and Reproductive Health, Chongqing Population and Family Planning Science and Technology Research Institute, Chongqing, PR China.
Int J Vitam Nutr Res. 2024 Jun;94(3-4):187-197. doi: 10.1024/0300-9831/a000786. Epub 2023 Jul 12.
Accumulating evidences have shown the beneficial effects of astaxanthin (AST) supplementation on metabolic diseases prevention and treatment. The goal of present study was to reveal the favorable interactions among AST supplementation, gut microbiota, and kidneys , so as to attenuate kidney impairment in diabetic mice. Twenty C57BL/6J mice were assigned to a normal control group and a diabetic model group induced by a high-fat diet plus low-dose streptozotocin, and then the diabetic mice were fed with a high-fat diet without or with AST [0.01% (AST_a) or 0.02% (AST_b)] for 12 weeks. When compared to the diabetes kidney disease (DKD) group, AST supplementation delayed the renal pathological progression, reduced fasting blood glucose (AST_b: 1.53-fold, <0.05), repressed levels of lipopolysaccharide (LPS; AST_a: 1.24-fold, =0.008; AST_b: 1.43-fold, <0.001) and TMAO (AST_a: 1.51-fold, =0.001; AST_b: 1.40-fold, =0.003), inhibited IL-6 (AST_a: 1.40-fold, =0.004; AST_b: 1.57-fold, =0.001) and reactive oxygen species (ROS; AST_a: 1.30-fold, =0.004; AST_b: 1.53-fold, <0.001), as well as regulated the Sirt1/PGC-1α/NFκB p65 signaling pathway. Moreover, the results of 16S rRNA gene-based Illumina deep sequencing in each group revealed that dietary AST supplementation also favorably modulated the gut microbiota compared with the DKD group, as evidenced by the inhibition of the harmful bacteria , and and the enhancement of the probiotics such as and . Taken together, dietary AST supplementation could protect kidneys against inflammation and oxidative stress by adjusting the gut-kidney axis in diabetic mice.
越来越多的证据表明，虾青素 (AST) 补充剂对代谢性疾病的预防和治疗有有益作用。本研究的目的是揭示 AST 补充剂、肠道菌群和肾脏之间的有利相互作用，以减轻糖尿病小鼠的肾脏损伤。将 20 只 C57BL/6J 小鼠分为正常对照组和高脂肪饮食加小剂量链脲佐菌素诱导的糖尿病模型组，然后用不含或含 AST[0.01%(AST_a)或 0.02%(AST_b)]的高脂肪饮食喂养糖尿病小鼠 12 周。与糖尿病肾病(DKD)组相比，AST 补充剂延缓了肾脏病理进展，降低了空腹血糖(AST_b：1.53 倍，<0.05)，抑制了脂多糖(LPS;AST_a：1.24 倍，=0.008；AST_b：1.43 倍，<0.001)和 TMAO(AST_a：1.51 倍，=0.001；AST_b：1.40 倍，=0.003)，抑制了白细胞介素-6(IL-6;AST_a：1.40 倍，=0.004；AST_b：1.57 倍，=0.001)和活性氧(ROS;AST_a：1.30 倍，=0.004；AST_b：1.53 倍，<0.001)，并调节了 Sirt1/PGC-1α/NFκB p65 信号通路。此外，每组基于 16S rRNA 基因的 Illumina 高通量测序结果表明，与 DKD 组相比，饮食 AST 补充剂还能很好地调节肠道菌群，这表现在有害菌的抑制，和益生菌的增强，如 和 。综上所述，饮食 AST 补充剂通过调节糖尿病小鼠的肠道-肾脏轴，可保护肾脏免受炎症和氧化应激的侵害。
