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白芍总苷通过抑制 ROS 积累和 PI3K/AKT 信号通路抑制破骨细胞生成和钛颗粒诱导的骨溶解。

Albiflorin inhibits osteoclastogenesis and titanium particles-induced osteolysis via inhibition of ROS accumulation and the PI3K/AKT signaling pathway.

机构信息

Department of Orthopedics, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu, China; Department of Orthopedics, Changshu Hospital Affiliated to Soochow University, First People's Hospital of Changshu City, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu, China; Department of Orthopedics, Central Laboratory, Changshu Hospital Affiliated to Soochow University, First People's Hospital of Changshu City, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu, China.

Department of Orthopedics, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu, China.

出版信息

Int Immunopharmacol. 2024 Dec 5;142(Pt B):113245. doi: 10.1016/j.intimp.2024.113245. Epub 2024 Sep 27.

Abstract

Periprosthetic osteolysis (PPO), caused by wear particles, is a significant complication of total joint replacement, leading to prosthesis failure. Previous research has highlighted the crucial role of osteoclast-induced bone destruction in PPO progression. Albiflorin (AF), a monoterpene glycoside from Paeonia lactiflora, is a key active ingredient known for its antioxidant and anti-inflammatory properties. Although AF has shown promise in treating various conditions, its impact on osteoclasts and PPO remains unexplored. Our study revealed that AF could effectively inhibit osteoclast differentiation to reduce overactivated bone resorption and effectively inhibit the accumulation of reactive oxygen species (ROS) induced by wear particles. In vitro experiments also confirmed that AF could effectively inhibit the PI3K/AKT signaling pathway and inhibit inflammation to regulate osteoclast generation. Studies in animal models have also verified the antioxidant and anti-inflammatory properties of AF. In summary, the above studies indicate that AF inhibits osteoclastogenesis via inhibiting ROS accumulation and the PI3K/AKT signaling pathway, which may be a potential therapeutic method for PPO.

摘要

假体周围骨溶解症(PPO)是全关节置换术的一种严重并发症,由磨损颗粒引起,可导致假体失效。先前的研究强调了破骨细胞诱导的骨破坏在 PPO 进展中的关键作用。白芍苷(AF)是从芍药中提取的一种单萜糖苷,具有抗氧化和抗炎特性,是一种关键的活性成分。尽管 AF 在治疗各种疾病方面显示出了潜力,但它对破骨细胞和 PPO 的影响仍未得到探索。我们的研究表明,AF 可以有效抑制破骨细胞分化,减少过度激活的骨吸收,并有效抑制磨损颗粒诱导的活性氧(ROS)的积累。体外实验还证实,AF 可以有效抑制 PI3K/AKT 信号通路,抑制炎症,从而调节破骨细胞的生成。动物模型研究也验证了 AF 的抗氧化和抗炎特性。综上所述,上述研究表明,AF 通过抑制 ROS 积累和 PI3K/AKT 信号通路抑制破骨细胞生成,这可能是治疗 PPO 的一种潜在方法。

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