Optimization of Astilbin Extraction from the Rhizome of Smilax glabra, and Evaluation of Its Anti-Inflammatory Effect and Probable Underlying Mechanism in Lipopolysaccharide-Induced RAW264.7 Macrophages

Molecules

Chuan-Li Lu¹  Yan-Fang Zhu²  Meng-Mei Hu²  Dong-Mei Wang¹  Xiao-Jie Xu¹  Chuan-Jian Lu¹  Wei Zhu¹ 

[1] Guangdong Provincial Academy of Chinese Medical Sciences, Guangzhou 510006, China; E-Mails:;School of Fundamental Medical Science, Guangzhou University of Chinese Medicine, Guangzhou 510120, China; E-Mails:

关键词: astilbin;    response surface methodology;    smilax glabra Rox;    anti-inflammatory;    inflammatory cytokine;    RAW264.7 cell;   

DOI  :  10.3390/molecules20010625

来源: mdpi

【 摘 要 】

Astilbin, a dihydroflavonol derivative found in many food and medicine plants, exhibited multiple pharmacological functions. In the present study, the ethanol extraction of astilbin from the rhizome of smilax glabra Roxb was optimized by response surface methodology (RSM) using Box-Behnken design. Results indicated that the obtained experimental data was well fitted to a second-order polynomial equation by using multiple regression analysis, and the optimal extraction conditions were identified as an extraction time of 40 min, ethanol concentration of 60%, temperature of 73.63 °C, and liquid-solid ratio of 29.89 mL/g for the highest predicted yield of astilbin (15.05 mg/g), which was confirmed through validation experiments. In addition, the anti-inflammatory efficiency of astilbin was evaluated in lipopolysaccharide (LPS)-induced RAW 264.7 cells. Results showed that astilbin, at non-cytotoxicity concentrations, significantly suppressed the production of nitric oxide (NO) and tumor necrosis factor-α (TNF-α), as well as the mRNA expression of inducible nitric oxide synthase (iNOS) and TNF-α in LPS-induced RAW 264.7 cells, but did not affect interleukin-6 (IL-6) release or its mRNA expression. These effects may be related to its up-regulation of the phosphorylation of p65, extracellular signal-regulated kinases 1/2 (ERK1/2) and c-Jun N-terminal kinase (JNK).

【 授权许可】

CC BY   
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