测定了64株赤芝(Ganoderma lucidum)子实体醇提物清除二苯基苦基苯肼(DPPH)自由基的活性和三萜指纹图谱,采用遗传算法筛选其指纹图谱中的26个共有峰,并标定出其中15个特征峰,运用偏最小二乘回归分析方法(partial least squares regressi...测定了64株赤芝(Ganoderma lucidum)子实体醇提物清除二苯基苦基苯肼(DPPH)自由基的活性和三萜指纹图谱,采用遗传算法筛选其指纹图谱中的26个共有峰,并标定出其中15个特征峰,运用偏最小二乘回归分析方法(partial least squares regression,PLSR)对指纹图谱中26个三萜峰与醇提物清除DPPH自由基的活性进行关联分析,建立了赤芝子实体三萜类化合物的抗氧化谱效关系方程。在赤芝子实体醇提物三萜指纹图谱的26个共有峰中,峰S1、S4、S9、S10和S26的峰面积与醇提物清除DPPH自由基的活性呈显著正相关关系;峰S3、S11、S15、S18、S19、S22和S25的峰面积与醇提物清除DPPH自由基的活性呈显著负相关关系。分别测定鉴定出的15个峰对应的三萜化合物对DPPH自由基的清除活性,发现与清除DPPH自由基活性呈显著正相关的三萜化合物灵芝酸C2(S4)、灵芝酸B(S9)、灵芝酸LM2(S10)、灵芝醛A(S26)对DPPH自由基的清除活性明显高于其他三萜化合物,与清除DPPH自由基活性呈显著负相关的三萜化合物灵芝酮三醇(S18)、灵芝萜酮二醇(S22)无清除DPPH自由基的活性。另外,利用H2O2诱导的PC12细胞损伤模型进一步验证灵芝酸C2、灵芝酸B、灵芝酸LM2、灵芝醛A和灵芝萜酮二醇在细胞水平的抗氧化活性,发现灵芝酸C2、灵芝酸B、灵芝酸LM2、灵芝醛A具有明显的保护神经细胞氧化损伤的活性,而灵芝萜酮二醇对神经细胞的氧化损伤无保护作用。结果表明,本研究建立的赤芝子实体三萜类化合物抗氧化谱效关系方程具有较高的准确性,能够较全面地反应赤芝子实体醇提物中不同三萜化合物与其抗氧化活性的相关性,可快速锁定有效成分以指导活性成分的分离纯化工作。此外,该方法也为赤芝子实体的质量控制提供了更为有效和准确的方法。展开更多
Objective: To investigate whether nitric oxide synthase (NOS) is expressed in T-cell-dependent liver injury initiated by concanavalin A (ConA) in Kunming mice and study the possible effect of nitric oxide(NO) on liver...Objective: To investigate whether nitric oxide synthase (NOS) is expressed in T-cell-dependent liver injury initiated by concanavalin A (ConA) in Kunming mice and study the possible effect of nitric oxide(NO) on liver injury models. Methods: Liver injury in Kunming mice was induced by administration of ConA through tail vein. Expression of NOS in the liver was detected by NADPH diaphorase staining method. The possible effect of NO on liver injury models was obtained by L-NAME injection to suppress synthesis of NO. Results: NOS has a strong expression in hepatocytes after ConA injection, especially in those close to the central vein, while only a weak expression was found in the epithelial cells in control group. Liver injury became more serious when NO synthesis was inhibited by L-NAME, accompanied by great malondialdehyde(MDA) increase in serum and severe intrahepatic vascular thrombosis. Conclusion: NOS markedly expressed in ConA-induced liver injury, which may subsequently promote nitric oxide synthesis. Increasement of nitric oxide has a protective effect on ConA-induced liver injury.展开更多
文摘测定了64株赤芝(Ganoderma lucidum)子实体醇提物清除二苯基苦基苯肼(DPPH)自由基的活性和三萜指纹图谱,采用遗传算法筛选其指纹图谱中的26个共有峰,并标定出其中15个特征峰,运用偏最小二乘回归分析方法(partial least squares regression,PLSR)对指纹图谱中26个三萜峰与醇提物清除DPPH自由基的活性进行关联分析,建立了赤芝子实体三萜类化合物的抗氧化谱效关系方程。在赤芝子实体醇提物三萜指纹图谱的26个共有峰中,峰S1、S4、S9、S10和S26的峰面积与醇提物清除DPPH自由基的活性呈显著正相关关系;峰S3、S11、S15、S18、S19、S22和S25的峰面积与醇提物清除DPPH自由基的活性呈显著负相关关系。分别测定鉴定出的15个峰对应的三萜化合物对DPPH自由基的清除活性,发现与清除DPPH自由基活性呈显著正相关的三萜化合物灵芝酸C2(S4)、灵芝酸B(S9)、灵芝酸LM2(S10)、灵芝醛A(S26)对DPPH自由基的清除活性明显高于其他三萜化合物,与清除DPPH自由基活性呈显著负相关的三萜化合物灵芝酮三醇(S18)、灵芝萜酮二醇(S22)无清除DPPH自由基的活性。另外,利用H2O2诱导的PC12细胞损伤模型进一步验证灵芝酸C2、灵芝酸B、灵芝酸LM2、灵芝醛A和灵芝萜酮二醇在细胞水平的抗氧化活性,发现灵芝酸C2、灵芝酸B、灵芝酸LM2、灵芝醛A具有明显的保护神经细胞氧化损伤的活性,而灵芝萜酮二醇对神经细胞的氧化损伤无保护作用。结果表明,本研究建立的赤芝子实体三萜类化合物抗氧化谱效关系方程具有较高的准确性,能够较全面地反应赤芝子实体醇提物中不同三萜化合物与其抗氧化活性的相关性,可快速锁定有效成分以指导活性成分的分离纯化工作。此外,该方法也为赤芝子实体的质量控制提供了更为有效和准确的方法。
文摘Objective: To investigate whether nitric oxide synthase (NOS) is expressed in T-cell-dependent liver injury initiated by concanavalin A (ConA) in Kunming mice and study the possible effect of nitric oxide(NO) on liver injury models. Methods: Liver injury in Kunming mice was induced by administration of ConA through tail vein. Expression of NOS in the liver was detected by NADPH diaphorase staining method. The possible effect of NO on liver injury models was obtained by L-NAME injection to suppress synthesis of NO. Results: NOS has a strong expression in hepatocytes after ConA injection, especially in those close to the central vein, while only a weak expression was found in the epithelial cells in control group. Liver injury became more serious when NO synthesis was inhibited by L-NAME, accompanied by great malondialdehyde(MDA) increase in serum and severe intrahepatic vascular thrombosis. Conclusion: NOS markedly expressed in ConA-induced liver injury, which may subsequently promote nitric oxide synthesis. Increasement of nitric oxide has a protective effect on ConA-induced liver injury.
