School of Pharmacy, Student Research Committee, Urmia University of Medical Sciences, Urmia, Iran.
Cellular and Molecular Research Center, Research Institute on Cellular and Molecular Medicine, Urmia University of Medical Sciences, Urmia, Iran.
BMC Gastroenterol. 2023 Sep 27;23(1):332. doi: 10.1186/s12876-023-02958-2.
Ulcerative Colitis (UC) is a disorder which oxidative stress plays a critical role in its pathogenesis. Empagliflozin (EMPA) is a sodium-glucose cotransporter-2 (SGLT2) inhibitor that has been shown to have anti-inflammatory and antioxidative effects. The aim of this study was to investigate the protective effects of EMPA on acetic acid (AA) induced colitis in rats.
A total of twenty-four rats were divided into four groups (six animals in each group) as follows: (1) Control group; (2) acetic acid (AA)-induced colitis group (AA); (3) EMPA treatment group (AA + EMPA); (4) Dexamethasone (Dexa) treatment group (AA + Dexa). Animals in pre-treatment groups received EMPA (10 mg/kg, i.p.) or dexamethasone (4 mg/kg, i.p. as reference drug) for four consecutive days before induction of colitis by intra-rectal acetic acid (4% v/v) administration. Twenty-four hours after AA administration, rats were sacrificed and the colon tissues were removed for histopathological and biochemical evaluations.
Pretreatment with EMPA significantly decreased colon weight/length ratio (81.00 ± 5.28 mg/cm vs. 108.80 ± 5.51 mg/cm) as well as, macroscopic (2.50 ± 0.57 vs. 3.75 ± 0.25) and histological scores (3.3 ± 0.14 vs. 1.98 ± 0.14) compared to the AA-induced colitis group (p < 0.01). Pretreatment with EMPA significantly reduced malondialdehyde (MDA) (324.0 ± 15.93 vs. 476.7 ± 32.26 nmol/mg p < 0.001) and increased glutathione level (117.5 ± 4.48 vs. 94.38 ± 3.950 µmol/mg, p < 0.01) in comparison to the AA-induced colitis group. Furthermore, a significant increase in catalase (44.60 ± 4.02 vs.14.59 ± 2.03 U/mg, P < 0.01), superoxide dismutase (283.9 ± 18.11 vs. 156.4 ± 7.92 U/mg, p < 0.001), and glutathione peroxidase (10.38 ± 1.45 vs. 2.508 ± 0.37, p < 0.01) activities were observed by EMPA pretreatment when compared to the AA-induced colitis group. These results were in line with those of the reference drug.
It is concluded that EMPA could effectively reduce the severity of tissue injury in experimental colitis. This protective effect may be related to the antioxidative effects of EMPA drug.
溃疡性结肠炎（UC）是一种疾病，其中氧化应激在其发病机制中起着关键作用。恩格列净（EMPA）是一种钠-葡萄糖共转运蛋白 2（SGLT2）抑制剂，已被证明具有抗炎和抗氧化作用。本研究旨在探讨 EMPA 对乙酸（AA）诱导的大鼠结肠炎的保护作用。
将 24 只大鼠分为四组（每组 6 只）：（1）对照组；（2）乙酸（AA）诱导的结肠炎组（AA）；（3）EMPA 治疗组（AA+EMPA）；（4）地塞米松（Dexa）治疗组（AA+Dexa）。在通过直肠内给予 4%（v/v）乙酸诱导结肠炎之前，预处理组的动物连续 4 天接受 EMPA（10mg/kg，ip）或地塞米松（4mg/kg，ip 作为参考药物）治疗。在 AA 给药后 24 小时，处死大鼠并取出结肠组织进行组织病理学和生化评估。
与 AA 诱导的结肠炎组相比，EMPA 预处理显著降低了结肠重量/长度比（81.00±5.28mg/cm 与 108.80±5.51mg/cm）以及宏观（2.50±0.57 与 3.75±0.25）和组织学评分（3.3±0.14 与 1.98±0.14）（p<0.01）。与 AA 诱导的结肠炎组相比，EMPA 预处理显著降低了丙二醛（MDA）（324.0±15.93 与 476.7±32.26 nmol/mg，p<0.001）并增加了谷胱甘肽水平（117.5±4.48 与 94.38±3.950 µmol/mg，p<0.01）。此外，与 AA 诱导的结肠炎组相比，EMPA 预处理时观察到过氧化氢酶（44.60±4.02 与 14.59±2.03 U/mg，P<0.01）、超氧化物歧化酶（283.9±18.11 与 156.4±7.92 U/mg，p<0.001）和谷胱甘肽过氧化物酶（10.38±1.45 与 2.508±0.37，p<0.01）的活性显著增加。这些结果与参考药物的结果一致。
EMPA 可有效减轻实验性结肠炎组织损伤的严重程度。这种保护作用可能与 EMPA 药物的抗氧化作用有关。
