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Deacetyl Ganoderic Acid F Inhibits LPS-Induced Neural Inflammation via NF-κB Pathway Both In Vitro and In Vivo
Nutrients ( IF 4.546 ) Pub Date : 2019-12-27 , DOI: 10.3390/nu12010085
Feiya Sheng , Lele Zhang , Songsong Wang , Lele Yang , Peng Li

Microglia mediated neuronal inflammation has been widely reported to be responsible for neurodegenerative disease. Deacetyl ganoderic acid F (DeGA F) is a triterpenoid isolated from Ganoderma lucidum, which is a famous edible and medicinal mushroom used for treatment of dizziness and insomnia in traditional medicine for a long time. In this study the inhibitory effects and mechanisms of DeGA F against lipopolysaccharide (LPS)-induced inflammation both in vitro and in vivo were investigated. On murine microglial cell line BV-2 cells, DeGA F treatment inhibited LPS-triggered NO production and iNOS expression and affected the secretion and mRNA levels of relative inflammatory cytokines. DeGA F inhibited LPS-induced activation of the NF-κB pathway, as evidenced by decreased phosphorylation of IKK and IκB and the nuclear translocation of P65. In vivo, DeGA F treatment effectively inhibited NO production in zebrafish embryos. Moreover, DeGA F suppressed the serum levels of pro-inflammatory cytokines, including TNF-α and IL-6 in LPS-stimulated mice model. DeGA F reduced inflammatory response by suppressing microglia and astrocytes activation and also suppressed LPS-induced NF-κB activation in mice brains. Taken together, DeGA F exhibited remarkable anti-inflammatory effects and promising therapeutic potential for neural inflammation associated diseases.

中文翻译:

脱乙酰基灵芝酸F通过体内和体外NF-κB途径抑制LPS诱导的神经炎症

小胶质细胞介导的神经元炎症已被广泛报道与神经退行性疾病有关。脱乙酰灵芝酸F(DeGA F)是从灵芝分离的三萜类化合物,灵芝是一种著名的食用和药用蘑菇,长期用于治疗传统医学中的头昏和失眠。在这项研究中,研究了DeGA F在体外和体内对脂多糖(LPS)诱导的炎症的抑制作用和机理。在鼠小神经胶质细胞系BV-2细胞上,DeGA F处理抑制LPS触发的NO产生和iNOS表达,并影响相关炎症细胞因子的分泌和mRNA水平。DeGA F抑制LPS诱导的NF-κB途径活化,这可通过IKK和IκB的磷酸化降低以及P65的核易位来证明。体内,DeGA F处理可有效抑制斑马鱼胚胎中的NO产生。此外,在脂多糖刺激的小鼠模型中,DeGA F抑制了血清促炎性细胞因子的水平,包括TNF-α和IL-6。DeGA F通过抑制小胶质细胞和星形胶质细胞的活化减少炎症反应,并且还抑制LPS诱导的小鼠脑中NF-κB活化。综上所述,DeGA F表现出了显着的抗炎作用,并有望在神经发炎相关疾病中具有广阔的治疗潜力。DeGA F通过抑制小胶质细胞和星形胶质细胞的活化减少炎症反应,并且还抑制LPS诱导的小鼠脑中NF-κB活化。综上所述,DeGA F表现出了显着的抗炎作用,并有望在神经发炎相关疾病中具有广阔的治疗潜力。DeGA F通过抑制小胶质细胞和星形胶质细胞的活化减少炎症反应,并且还抑制LPS诱导的小鼠脑中NF-κB活化。综上所述,DeGA F表现出了显着的抗炎作用,并有望在神经发炎相关疾病中具有广阔的治疗潜力。
更新日期:2019-12-27
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