期刊文献+

三七多糖对氧化损伤衰老模型小鼠的抗氧化活性及脏器保护作用研究 被引量:1

Antioxidant activity and organ protection of Panax notoginseng polysaccharide on oxidative damage and aging model mice
原文传递
导出
摘要 目的研究三七多糖(PNPS)不同组分在D-半乳糖致氧化损伤衰老模型小鼠体内的抗氧化活性及其脏器保护作用。方法将KM小鼠随机分为正常组、模型组、维生素C(VC)组(给予200 mg·kg^(-1) VC)、粗多糖(CPPN)组、中性多糖(NPPN)组和酸性多糖(APPN-Ⅰ、APPN-Ⅱ、APPN-Ⅲ)组(分别给予400 mg·kg^(-1) CPPN、NPPN、APPN-Ⅰ、APPN-Ⅱ、APPN-Ⅲ)。除正常组外,均用腹腔注射1 g·kg^(-1) D-半乳糖方法建立氧化损伤衰老小鼠模型。连续给药42 d后处死小鼠,制备血清和肝匀浆。用硫代巴比妥酸法测定丙二醛(MDA)含量;用四唑盐法测定超氧化物歧化酶(SOD)含量;用双抗体夹心法测定谷胱甘肽过氧化物酶(GSH-Px)含量。结果正常组、模型组、VC组、CPPN组、NPPN组、APPN-Ⅰ组、APPN-Ⅱ组和APPN-Ⅲ组血清SOD分别为(15.07±0.69)、(12.79±1.51)、(15.56±1.01)、(13.69±0.96)、(14.27±0.64)、(14.31±0.99)、(14.18±0.79)和(15.85±0.89)U·mL^(-1),血清GSH-Px分别为(105.35±4.97)、(90.36±4.31)、(111.51±7.00)、(113.03±8.06)、(118.77±5.19)、(123.60±8.08)、(131.65±3.60)和(149.22±13.32)ng·L^(-1),血清MDA分别为(1.72±0.26)、(4.16±0.92)、(2.26±0.59)、(2.82±0.47)、(2.46±0.50)、(1.98±0.41)、(2.39±0.39)和(2.07±0.24)nmol·mL^(-1),肝SOD分别为(234.22±3.84)、(205.04±7.28)、(234.63±6.37)、(214.99±17.66)、(234.13±3.63)、(234.63±3.44)、(233.87±5.63)和(235.42±2.33)U·mgprot^(-1),肝GSH-Px分别为(274.27±23.72)、(207.00±15.22)、(257.68±16.39)、(249.79±18.78)、(252.62±10.92)、(256.25±21.83)、(261.20±17.52)和(263.16±17.98)ng·L^(-1),肝MDA分别为(35.70±3.52)、(49.65±6.32)、(36.15±2.48)、(39.17±4.29)、(37.40±6.19)、(35.34±4.06)、(35.90±5.36)和(33.31±7.64)nmol·mgprot^(-1)。模型组与正常组比较,小鼠血清和肝中的SOD、GSH-Px均显著降低,MDA含量显著升高(均P<0.01)。经三七多糖不同组分治疗后,小鼠体内氧化指标明显改善,其中APPN-Ⅲ抗氧化活性最好,可提高血清和肝中的SOD、GSH-Px活性,降低MDA的含量(均P<0.01)。结论三七多糖不同组分在体内均有抗氧化活性和脏器保护作用,其中APPN-Ⅲ的抗氧化活性最好,有很好的脏器保护作用。 Objective To study the antioxidant activity and organ protection of different components of Panax notoginseng polysaccharide(PNPS)in D-galactose-induced oxidative damage aging model mice.Methods KM mice were randomly divided into normal group,model group,vitamin C(VC)group(given 200 mg·kg^(-1) VC),crude polysaccharide from Panax notoginseng(CPPN)group,neutral polysaccharide from Panax notoginseng(NPPN)group and acidic polysaccharide from Panax notoginseng(APPN-Ⅰ,APPN-Ⅱ,APPN-Ⅲ)group(given 400 mg·kg^(-1) CPPN,NPPN,APPN-Ⅰ,APPN-Ⅱ,APPN-Ⅲ,respectively).Except for the normal group,oxidative injury aging mouse models were established by intraperitoneal injection of 1 g·kg^(-1) D-galactose.The mice were sacrificed after continuous administration for 42 days,and serum and liver homogenate were prepared.Malondialdehyde(MDA)was determined by thiobarbituric acid method;superoxide dismutase(SOD)was determined by tetrazole salt method;glutathione peroxidase(GSH-Px)was determined by double antibody sandwich method.Results Serum SOD in the normal group,model group,VC group,CPPN group,NPPN group and APPN-Ⅰ,APPN-Ⅱ,APPN-Ⅲ groups were(15.07±0.69),(12.79±1.51),(15.56±1.01),(13.69±0.96),(14.27±0.64),(14.31±0.99),(14.18±0.79)and(15.85±0.89)U·mL^(-1);serum GSH-Px were(105.35±4.97),(90.36±4.31),(111.51±7.00),(113.03±8.06),(118.77±5.19),(123.60±8.08),(131.65±3.60)and(149.22±13.32)ng·L^(-1);serum MDA were(1.72±0.26),(4.16±0.92),(2.26±0.59),(2.82±0.47),(2.46±0.50),(1.98±0.41),(2.39±0.39)and(2.07±0.24)nmol·mL^(-1);the liver SOD were(234.22±3.84),(205.04±7.28),(234.63±6.37),(214.99±17.66),(234.13±3.63),(234.63±3.44),(233.87±5.63)and(235.42±2.33)U.mgprot-1;liver GSH-Px were(274.27±23.72),(207.00±15.22),(257.68±16.39),(249.79±18.78),(252.62±10.92),(256.25±21.83),(261.20±17.52)and(263.16±17.98)ng·L^(-1);liver MDA were(35.70±3.52),(49.65±6.32),(36.15±2.48),(39.17±4.29),(37.40±6.19),(35.34±4.06)and(35.90±5.36),(33.31±7.64)nmol·mgprot^(-1).Compared with the normal group,SOD,GSH-Px in serum and liver of mice in the model group were significantly reduced,and the content of MDA was significantly increased(all P<0.01).After treatment with different components of Panax notoginseng polysaccharide,the oxidative indicators in mice were significantly improved,among which APPN-Ⅲ have the best antioxidant activity,which could significantly increase the activities of SOD,GSH-Px in serum and liver,and reduce the content of MDA(all P<0.01).Conclusion Different components of Panax notoginseng polysaccharide have antioxidant activity and organ protection in vivo,among which APPN-Ⅲ has the best antioxidant activity and has a good organ protection effect.
作者 邓萌玥 位盼盼 李铭 晏子俊 夏谍 丁俞珍 张磊 陈彤 DENG Meng-yue;WEI Pan-pan;LI Ming;YAN Zi-jun;XIA Die;DING Yu-zhen;ZHANG Lei;CHEN Tong(School of Pharmaceutical Sciences and Yunnan Key Laboratory of Pharmacology for Natural Products,Kunming Medical University,Kunming 650500,Yunnan Province,China;School of Rehabilitation,Kunming Medical University,Kunming 650500,Yunnan Province,China;Pharmacy Department,First People’s Hospital of Xuanwei City,Xuanwei 655400,Yunnan Province,China;Department of Ultrasound Medicine,The Third Affiliated Hospital of Kunming Medical University,Kunming 650118,Yunnan Province,China)
出处 《中国临床药理学杂志》 CAS CSCD 北大核心 2024年第6期889-893,共5页 The Chinese Journal of Clinical Pharmacology
基金 国家自然科学基金地区科学基金资助项目(81760698) 第七批云南省高校工程研究中心立项建设基金资助项目([2019]-57) 云南省“兴滇英才支持计划”教学名师基金资助项目(60122090101)。
关键词 三七多糖 不同组分 衰老模型小鼠 抗氧化活性 脏器保护 Panax notoginseng polysaccharides different components aging model mice antioxidant activity organ protection
  • 相关文献

参考文献2

二级参考文献6

  • 1Anil K,Jaiswal AK. Nr.2/INr.2 ( Keapl ) Signaling in oxidative stressand cellular protection [ J/OL ]. Free Radic Biol Med,2009,47 ( 9 ):1304.
  • 2张艳磊,何晓然,刘园园,等.金钗石斛对高糖诱导的人肾系膜细胞氧化应激损伤的影响[J].时珍国医国药,2012,23(12) :42.
  • 3Kobayashi A ,Kang M I, Okawa H ,et al. Oxidative stress sensor Keaplfunctions as an adaptor for Cul3 based E3 ligase toregulate proteasomaldegradation of Nr.2[J].Mol Cell Biol,2004,24(16) :7130.
  • 4Furukawa M, Xiong Y. BTB protein Keapl targets antioxidam transcrip-tion factor Nrf2 for ubiquitination hy the Cullin3 - Rod ligase[ J]. MolCell Biol,2005,25(1) :162.
  • 5Pergola PE,Raskin P,Toto RD,et al. Bardoxolone methyl and kidneyfunction in CKD with type 2 diabetes [ J ]. N Engl J Med, 2011,365(4):327.
  • 6Holland R,Hawkins AE,Eggler AL,et al. Prospective type 1 and type 2disulfides of Keapl protein [ J]. Chem Res Toxicol,2008, 21 ( 10 ):2051.

共引文献18

同被引文献13

引证文献1

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部