LIU Hengge, XU Xinxing, BAI Fan, et al. Optimization of Sturgeon Cartilage Products and Its Regulation on Human Chondrocyte Inflammation[J]. Science and Technology of Food Industry, 2022, 43(15): 165−174. (in Chinese with English abstract). doi: 10.13386/j.issn1002-0306.2021100051.
Citation: LIU Hengge, XU Xinxing, BAI Fan, et al. Optimization of Sturgeon Cartilage Products and Its Regulation on Human Chondrocyte Inflammation[J]. Science and Technology of Food Industry, 2022, 43(15): 165−174. (in Chinese with English abstract). doi: 10.13386/j.issn1002-0306.2021100051.

Optimization of Sturgeon Cartilage Products and Its Regulation on Human Chondrocyte Inflammation

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  • Received Date: October 11, 2021
  • Available Online: June 18, 2022
  • The purpose of this paper was to prepare a sturgeon cartilage product from sturgeon cartilage and explore its effect on inflammation of human chondrocytes. A kind of sturgeon cartilage product was prepared by thermal liquefaction of sturgeon cartilage and dragon tendon at high temperature and high pressure. The optimum preparation conditions were determined by single factor and orthogonal test. Human chondrocytes were cultured by preparing drug-containing serum and the effects of sturgeon cartilage products on Interleukin 1β (IL-1β)-induced cell inflammatory model were investigated by MTT, Alsinland staining and ELISA. The results showed that the best preparation conditions of sturgeon cartilage products were as follows: Hot liquefaction temperature was 120 ℃, hot liquefaction time was 20 min, boiling temperature was 80 ℃, boiling time was 30 min. Under this condition, the sensory score of the product was 59.69. The drug-containing serum of sturgeon cartilage products group had no cytotoxicity and could stimulate chondrocytes to secrete collagen and proteoglycan and other extracellular matrix. Meanwhile, the product could significantly increase the proliferation activity of inflammatory cells by 156% (P<0.05), and significantly inhibited the expression levels of NO, INOS, IL-6, COX-2 and PGE2 in the inflammatory chondrocytes (P<0.05).
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