从杜仲中提取的木脂素。防止AGEs诱导的视网膜内皮细胞损伤。

PubMed ID
G H
发表日期 2016年月

原始出处 细胞生理学和生物化学:国际实验细胞生理学、生物化学和药理学杂志
Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology
作者 Liu  Ban  Li  Chao-Peng  Wang  Wen-Qi  Song  Shu-Guang  Liu  Xiu-Ming 

文献标题 从杜仲中提取的木脂素。防止AGEs诱导的视网膜内皮细胞损伤。
Lignans Extracted from Eucommia Ulmoides Oliv. Protects Against AGEs-Induced Retinal Endothelial Cell Injury.
Lignans Extracted from Eucommia Ulmoides Oliv. Protects Against AGEs-Induced Retinal Endothelial Cell Injury.

文献摘要 BACKGROUND/AIMS

晚期糖基化终产物(AGEs)在糖尿病视网膜病变(DR)等缺血性视网膜病变中可引起氧化应激,触发和加重内皮损伤。杜仲叶又名杜仲、杜仲,用于治疗高血压和糖尿病,具有很强的抗氧化和抗糖基化活性。木脂素是杜仲的主要生物活性成分之一。本研究主要探讨木脂素对AGEs诱导的内皮损伤的影响。

METHODS

MTT法、Hoechst染色和钙黄绿素AM/碘化丙啶(PI)染色检测木脂素对内皮细胞功能的影响。视网膜胰蛋白酶消化、伊文思蓝试验、异凝集素染色和westernblots检测木脂素对视网膜微血管功能的影响。采用westernblot、蛋白免疫沉淀法(IP)、MTT法和酶活性测定法检测配体处理对氧化应激反应的影响。

RESULTS

木脂素对体外AGEs诱导的视网膜内皮细胞损伤和体内糖尿病诱导的血管功能障碍具有保护作用。木脂素治疗可调节视网膜内皮细胞系、视网膜和肝脏的氧化应激反应。此外,我们还发现NRF2/HO-1信号对木脂素介导的氧化应激调节至关重要。

CONCLUSION

木脂素治疗可通过调节Nrf2/HO-1信号通路在体内外保护血管内皮功能。木脂素有望成为治疗糖尿病微血管功能障碍的有效药物。


BACKGROUND/AIMS

Advanced glycation end products (AGEs) could elicit oxidative stress, trigger and aggravate endothelium damage in several ischemic retinopathies including diabetic retinopathy (DR). The leaves of Eucommia ulmoides O., also referred to as Tu-chung or Du-zhong, have been used for the treatment of hypertension and diabetes, showing great antioxidant activity and anti-glycation activity. Lignans is one of the main bioactive components of Eucommia ulmoides. This study mainly investigated the effect of lignans treatment on AGEs-induced endothelium damage.

METHODS

MTT assay, Hoechst staining, and calcein-AM/ propidium iodide (PI) staining was conducted to determine the effect of lignans treatment on endothelial cell function in vitro. Retinal trypsin digestion, Evans blue assay, isolectin staining, and western blots were conducted to determine the effect of lignans treatment on retinal microvascular function in vivo. Western blot, protein immunoprecipitation (IP), MTT assays, and enzyme activity assay was conducted to detect the effect of ligans treatment on oxidative stress response.

RESULTS

Lignans protected retinal endothelial cell against AGEs-induced injury in vitro and diabetes-induced vascular dysfunction in vivo. Lignans treatment could regulate oxidative stress response in retinal endothelial cell line, retina, and liver. Moreover, we showed that NRF2/HO-1 signaling was critical for lignans-mediated oxidative stress regulation.

CONCLUSION

Lignans treatment could protect against endothelial dysfunction in vivo and in vitro via regulating Nrf2/HO-1 signaling. Lignans might be developed as a promising drug for the treatment of diabetes-induced microvascular dysfunction.

BACKGROUND/AIMS

Advanced glycation end products (AGEs) could elicit oxidative stress, trigger and aggravate endothelium damage in several ischemic retinopathies including diabetic retinopathy (DR). The leaves of Eucommia ulmoides O., also referred to as Tu-chung or Du-zhong, have been used for the treatment of hypertension and diabetes, showing great antioxidant activity and anti-glycation activity. Lignans is one of the main bioactive components of Eucommia ulmoides. This study mainly investigated the effect of lignans treatment on AGEs-induced endothelium damage.

METHODS

MTT assay, Hoechst staining, and calcein-AM/ propidium iodide (PI) staining was conducted to determine the effect of lignans treatment on endothelial cell function in vitro. Retinal trypsin digestion, Evans blue assay, isolectin staining, and western blots were conducted to determine the effect of lignans treatment on retinal microvascular function in vivo. Western blot, protein immunoprecipitation (IP), MTT assays, and enzyme activity assay was conducted to detect the effect of ligans treatment on oxidative stress response.

RESULTS

Lignans protected retinal endothelial cell against AGEs-induced injury in vitro and diabetes-induced vascular dysfunction in vivo. Lignans treatment could regulate oxidative stress response in retinal endothelial cell line, retina, and liver. Moreover, we showed that NRF2/HO-1 signaling was critical for lignans-mediated oxidative stress regulation.

CONCLUSION

Lignans treatment could protect against endothelial dysfunction in vivo and in vitro via regulating Nrf2/HO-1 signaling. Lignans might be developed as a promising drug for the treatment of diabetes-induced microvascular dysfunction.


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