徐 慧,回广飞,张一恺,尚沛津,刘天龙,丁 一,刘文星,朱志会,王明明,李玉文,文爱东.11-羰基-β-乙酰乳香酸抗氧化胃保护作用及机制研究[J].现代生物医学进展英文版,2017,17(20):3816-3820. |
11-羰基-β-乙酰乳香酸抗氧化胃保护作用及机制研究 |
Antioxidant Mediated Preventative Effect of Acetyl-11-Keto-beta-Boswellic Acid on Gastric Injury in Rats |
Received:January 05, 2017 Revised:January 29, 2017 |
DOI:10.13241/j.cnki.pmb.2017.20.004 |
中文关键词: 11-羰基-β-乙酰乳香酸 抗氧化 胃溃疡 |
英文关键词: Acetyl-11-Keto-beta-Boswellic Acid (AKBA) Anti-oxidant Gastric ulcer |
基金项目:国家自然科学基金项目(81373947;81201985) |
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中文摘要: |
摘要 目的:研究11-羰基-β-乙酰乳香酸(AKBA)的抗氧化作用及胃保护效果。方法:30只SD大鼠随机分为5组:正常组(生理盐水5 mL/kg),模型组(吲哚美辛48 mg/kg),西咪替丁组(100 mg/kg),低剂量AKBA组(100 mg/kg),高剂量AKBA组(200 mg/kg)。预给药1小时后,用吲哚美辛(48 mg/kg)灌胃造模,评价溃疡指数(UI)、胃内容物酸度(pH)、胃壁黏液量(GWM)、前列腺素E2(PGE-2)及一氧化氮(NO)的含量,并检测超氧化物歧化酶(SOD)、过氧化氢酶(CAT)的活性,丙二醛(MDA)含量及核转录相关因子2(Nrf2)和血红素加氧酶1(HO-1)的表达量。结果:①与造模组相比,AKBA高剂量组(P<0.05)与西咪替丁组(P<0.001)显著降低了吲哚美辛诱导的胃粘膜损伤,AKBA低剂量组的差异无统计学意义;②AKBA与西咪替丁均显著升高胃内容物pH(P<0.001)(AKBA低剂量组P<0.05),增加GWM含量(P<0.001);③与造模组相比,AKBA及西咪替丁组均显著增高PGE-2及NO含量(P<0.001);④与造模组相比,AKBA及西咪替丁组均显著增高SOD活性(P<0.001)(AKBA低剂量组P<0.05)及CAT活性(P<0.001)并降低了MDA含量(P<0.001);⑤与造模组相比,AKBA高剂量组及西咪替丁组促进Nrf2及HO-1表达明显增高(P<0.05)。结论:AKBA有较好的胃保护效果,同时可以通过升高GWM、降低胃内容物pH,升高NO含量,阻止PGE-2的降低,同时恢复SOD、CAT的活性,降低MDA含量,促进Nrf2及HO-1的表达发挥胃黏膜保护的作用。 |
英文摘要: |
ABSTRACT Objective: To investigate the protective effect and antioxidant effect of Acetyl-11-Keto-beta-Boswellic Acid (AKBA) in gastric injury in rats. Methods: All the 30 rats were divided evenly and randomly into the following 5 groups: control group (5 mL/kg physiological saline), model group (5 mL/kg physiological saline), cimetidine group (100 mg/kg), L-AKBA group (100 mg/kg) and H-AKBA group (200 mg/kg). One hour before administration of indomethacin, the vehicle, cimetidine and AKBA were given to each experimental group through administration by gavage. The gastro-protection effect was assessed by measuring ulcer index (UI), gastric juice acidity (pH), gastric wall mucus (GWM), prostaglandin E2 (PGE-2) and nitric oxide (NO). The antioxidant effects were measured through the activity of superoxide dismutase (SOD), catalase (CAT) and the level of MDA. Meanwhile, the expression of Erythroid-2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) were assessed. Results: ① Compared with model group, UI was decreased significantly in H-AKBA group (P<0.05) and cimetidine group (P<0.001), while the difference between L-AKBA group and model group were not statistical significance; ② Compared with model group, and the GWM were increased markedly in both AKBA groups and cimetidine group (P<0.001), and pH were increased in H-AKBA group, cimetidine group (P<0.001) and L-AKBA group (P<0.05); ③ Compared with control group, the level of PGE-2 and NO were significantly increased in both AKBA groups and cimetidine group (P<0.001). ④ Compared with model group, the activity of SOD and CAT were increased in H-AKBA group, cimetidine group (P<0.001), and in L-AKBA group (P<0.05). Besides, the level of MDA were decreased in both AKBA groups and cimetidine group (P<0.001). ⑤ The expression of Nrf2 and HO-1 were increased in H-AKBA group, cimetidine group (P<0.05). Conclusion: The AKBA could protect gastric from injury through increasing GWM and gastric juice acidity and the level of PGE-2 and NO. Besides, AKBA could prevent gastric from oxidative stress through increase the activity of SOD and CAT, and decrease the level of MDA. Meanwhile, AKBA could promote the expression of Nrf2 and HO-1 to protect gastric from acute injury. |
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