关键词: Brazilian propolis endoplasmic reticulum stress kaempferol nonalcoholic fatty liver disease oxidative stress

Mesh : Propolis / pharmacology therapeutic use Animals Endoplasmic Reticulum Stress / drug effects Humans Non-alcoholic Fatty Liver Disease / drug therapy pathology metabolism Hep G2 Cells Oxidative Stress / drug effects Male Liver / drug effects pathology metabolism Apoptosis / drug effects Mice Kaempferols / pharmacology therapeutic use Brazil Cell Proliferation / drug effects Mice, Inbred C57BL

来  源:   DOI:10.1248/bpb.b24-00092

Abstract:
There is evidence that propolis exhibits anti-inflammatory, anticancer, and antioxidant properties. We assessed the potential beneficial effects of Brazilian propolis on liver injury in nonalcoholic fatty liver disease (NAFLD). Our findings demonstrate that Brazilian propolis suppresses inflammation and fibrosis in the liver of mice with NAFLD by inhibiting the expression of genes involved in endoplasmic reticulum (ER) stress. Additionally, Brazilian propolis also suppressed the expression of ER stress-related genes in HepG2 cells treated with an excess of free fatty acids, leading to cell apoptosis. A deeper analysis revealed that kaempferol, one of the components present in Brazilian propolis, induces cell proliferation through the mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase (ERK) pathway and protects against oxidative stress. In conclusion, Brazilian propolis exhibits hepatoprotective properties against oxidative stress by inhibiting ER stress in NAFLD-induced model mice.
摘要:
有证据表明蜂胶具有抗炎作用,抗癌,和抗氧化性能。我们评估了巴西蜂胶对非酒精性脂肪性肝病(NAFLD)肝损伤的潜在有益作用。我们的发现表明,巴西蜂胶通过抑制内质网(ER)应激相关基因的表达来抑制NAFLD小鼠肝脏的炎症和纤维化。此外,巴西蜂胶还抑制了用过量游离脂肪酸处理的HepG2细胞中ER应激相关基因的表达,导致细胞凋亡。更深入的分析表明山奈酚,巴西蜂胶中存在的成分之一,通过丝裂原活化蛋白激酶(MAPK)/细胞外信号调节激酶(ERK)途径诱导细胞增殖,并防止氧化应激。总之,巴西蜂胶在NAFLD诱导的模型小鼠中通过抑制ER应激表现出针对氧化应激的保肝特性。
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