Polydopamine nanoparticles as dual-task platform for osteoarthritis therapy: A scavenger for reactive oxygen species and regulator for cellular powerhouses
Polydopamine nanoparticles as dual-task platform for osteoarthritis therapy: A scavenger for reactive oxygen species and regulator for cellular powerhouses
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聚多巴胺纳米颗粒作为骨关节炎治疗的双任务平台:活性氧的清除剂和细胞动力室的调节剂
DOI:
10.1016/j.cej.2021.129284
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发表时间:
2021-08
影响因子:
15.1
通讯作者:
Shen Steve G.
中科院分区:
文献类型:
--
作者:
Wang Xiangyu;Zhao Hanjiang;Liu Zhenchuan;Wang Yitong;Lin Dan;Chen Long;Dai Jiewen;Lin Kaili;Shen Steve G.
Because of the obscure etiology of osteoarthritis (OA) and unsatisfactory treatment outcomes, new effective and minimally invasive therapies are urgently needed. Oxidative stress elicited by excessive reactive oxygen species (ROS) accumulation has historically been considered a potential trigger of OA. Polydopamine (PDA), an emerging versatile biopolymer produced by self-polymerization of dopamine, has attracted considerable attention in biomedical applications by virtue of its excellent biocompatibility and intriguing ROS-scavenging capacity. Herein, an antioxidative/anti-inflammatory dual-task nanoplatform based on PDA nanoparticles (NPs) is introduced for the treatment of temporomandibular joint osteoarthritis (TMJ-OA). In addition to directly reacting with ROS as a reducing agent, PDA NPs also regulate ROS generation in mitochondria which are considered cellular powerhouses. Specifically, the efficiency of mitochondrial oxidative phosphorylation (OXPHOS) is significantly increased in the presence of PDA NPs, indicating that PDA NPs may increase the efficiency of mitochondrial respiration, hence reducing ROS production. This intriguing dual-antioxidative mechanism may account for the remarkable antioxidative capacity of PDA NPs. Moreover, the anti-inflammatory capacity of PDA NPs is revealed bothin vitroandin vivo. This work not only opens a new avenue for OA treatment but also provides valuable insights into the design of biomaterials with multiple biomedical applications via regulation of cellular energy metabolism.
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影响因子:
3.3
作者:
Gollmer, Anita;Arnbjerg, Jacob;Ogilby, Peter R.
通讯作者:
Ogilby, Peter R.
DOI:
10.1007/978-3-030-39982-5_7
发表时间:
2020
期刊:
Pain Management for Clinicians
影响因子:
--
作者:
Nilofar Syed;Una E. Makris
通讯作者:
Nilofar Syed;Una E. Makris
影响因子:
5.6
作者:
Hu Q;Ecker M
通讯作者:
Ecker M
影响因子:
64.5
作者:
TOLEDANO, MB;KULLIK, I;STORZ, G
通讯作者:
STORZ, G
DOI:
10.1016/s0889-5406(05)81195-3
发表时间:
1992
期刊:
American journal of orthodontics and dentofacial orthopedics : official publication of the American Association of Orthodontists, its constituent societies, and the American Board of Orthodontics
影响因子:
--
作者:
J. Okun
通讯作者:
J. Okun