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生的 ROS,抑制氧化应激的水平,进而延缓糖尿病肾病                               dants melatonin,vitamin D and vitamin E in diabetic rats
          患者肾小球硬化和肾小管间质纤维化 。因此,本研究                                 [J]. J Taibah Univ Med Sci,2020,15(5):351-357.
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          采用高脂饮食联合腹腔注射 STZ 诱导糖尿病肾病模型                          [ 7 ]  HASHEMI  M,ZANDIEH  M A,ZIAOLHAGH  S,et  al.
          小鼠,并以维生素 E 为阳性对照。本研究结果显示,与                               Nrf2  signaling  in  diabetic  nephropathy,cardiomyopathy
          正常对照组相比,模型组小鼠系膜基质堆积、肾小球硬                                 and  neuropathy:therapeutic  targeting,challenges  and  fu‐
          化、肾小管间质纤维化明显,肾脏系数、肾功能相关指标                                ture prospective[J]. Biochim Biophys Acta Mol Basis Dis,
          水平和 MDA、8-OHdG 含量均显著升高,SOD、GSH-Px                        2023,1869(5):166714.
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          含量均显著降低;经TAB干预后,上述指标均显著改善,                               fects  of  Scoparia  dulcis  L.  extract  on  high  glucose-
          这提示TAB可改善糖尿病肾病模型小鼠的肾功能、氧化                                induced injury in human retinal pigment epithelial cells[J].
          应激水平、肾小管间质纤维化。                                           Front Nutr,2023,10:1085248.
              在糖尿病肾病中,高血糖和氧化应激会导致肾脏内                          [ 9 ]  CHI C W,WANG C N,LIN Y L,et al. Tournefolic acid B
          ECM沉积相关因子的异常积聚,伴随着肾小球硬化和肾                                methyl  ester  attenuates  glutamate-induced  toxicity  by
          小管间质纤维化,从而加剧了肾脏损伤。Akt/Nrf2/HO-1                          blockade of ROS accumulation and abrogating the activa‐
          信号通路是重要的细胞保护通路,可对抗氧化应激,减                                 tion of caspases and JNK in rat cortical neurons[J]. J Neu‐
          轻细胞受损。在糖尿病肾病中,该信号通路的活性通常                                 rochem,2005,92(3):692-700.
          受到抑制,导致细胞对氧化应激的抵抗力下降                     [4—5] 。本   [10]  LI X ,XU B,WU J,et al. Maresin 1 alleviates diabetic
          研究结果显示,经 TAB 干预后,小鼠肾组织中 TGF-β1、                          kidney  disease  via  LGR6-mediated  cAMP-SOD2-ROS
          Fn、Col Ⅳ蛋白表达水平均显著降低,p-Akt、Nrf2、HO-1                      pathway[J]. Oxid Med Cell Longev,2022,19(4):7177889.
          蛋白表达水平均显著升高,这提示TAB可通过激活Akt/                         [11]  BAI X,LI X,TIAN J,et al. A new model of diabetic ne‐
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          Nrf2/HO-1 信号通路,减少肾组织 ECM 沉积,进而减缓
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          糖尿病肾病的进展。                                                118:71-84.
              综上所述,TAB可改善糖尿病肾病模型小鼠糖代谢
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          和肾功能,减轻肾小管间质纤维化;其作用机制可能与                                 bits  HFD/STZ-induced  diabetic  nephropathy  via  inflam‐
          激活 Akt/Nrf2/HO-1 信号通路,抑制 ECM 沉积,拮抗高                      matory and apoptotic signaling pathways in C57BL/6 mice
          糖诱导的氧化应激有关。                                              [J]. J Ethnopharmacol,2023,314:116596.
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          · 2860 ·    China Pharmacy  2023 Vol. 34  No. 23                            中国药房  2023年第34卷第23期
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