1. Academic Validation
  2. Exosomes derived from baicalin‑pretreated mesenchymal stem cells mitigate atherosclerosis by regulating the SIRT1/NF‑κB signaling pathway

Exosomes derived from baicalin‑pretreated mesenchymal stem cells mitigate atherosclerosis by regulating the SIRT1/NF‑κB signaling pathway

  • Mol Med Rep. 2025 May;31(5):126. doi: 10.3892/mmr.2025.13491.
Xiaochun Yang # 1 Wei Wu # 1 Weitian Huang 2 Junfeng Fang 3 Yunli Chen 2 Xiaoyan Chen 2 Xiaolan Lin 2 Yanbin He 2
Affiliations

Affiliations

  • 1 The First Clinical College of Medicine, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong 510405, P.R. China.
  • 2 Department of Rehabilitation, Guangdong Work Injury Rehabilitation Hospital, Guangzhou, Guangdong 510000, P.R. China.
  • 3 Department of Emergency, The First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, Guangdong 510000, P.R. China.
  • # Contributed equally.
Abstract

Atherosclerosis (AS) is a disease with high global incidence and mortality rates. Currently, the treatment of AS in clinical practice carries a high risk of adverse effects and toxic side effects. The pretreatment of mesenchymal stem cells (MSCs) with drugs may enhance the bioactivity of MSC‑derived exosomes (MSC‑exos), which could be a promising candidate for inhibiting the progression of AS. The aim of the present study was to investigate the ability of exos derived from baicalin‑preconditioned MSCs (Ba‑exos) to exhibit an inhibitory effect on AS progression and to explore the potential molecular mechanisms. Exos were isolated from untreated MSCs and MSCs pretreated with Ba, and were characterized using transmission electron microscopy, nanoparticle tracking analysis and western blotting. Subsequently, Cell Counting Kit‑8 and Transwell assays, reverse transcription‑quantitative PCR, immunofluorescence, western blotting and ELISA were used to evaluate the effects of Ba‑exos on AS, and the possible molecular mechanisms. Oil Red O and Masson staining were used to assess AS pathological tissue in a high‑fat diet‑induced mouse model of AS. Notably, MSC‑exos and Ba‑exos were successfully isolated. Compared with MSC‑exos, Ba‑exos demonstrated superior inhibitory effects on the viability and migration, and the levels of inflammatory factors in oxidized low‑density lipoprotein (ox‑LDL)‑induced vascular smooth muscle cells (VSMCs). Additionally, compared with MSC‑exos, Ba‑exos significantly inhibited NF‑κB activation by upregulating Sirtuin 1 (SIRT1), thereby suppressing inflammation in ox‑LDL‑induced VSMCs to a greater extent. In mice with high‑fat diet‑induced AS, Ba‑exos exhibited the ability to inhibit AS plaque formation and to alleviate AS progression by reducing the levels of inflammatory factors compared with MSC‑exos; however, the difference was not significant. In conclusion, Ba‑exos may serve as a potential strategy for treating AS by regulating the SIRT1/NF‑κB signaling pathway to suppress inflammation.

Keywords

atherosclerosis; baicalin; exosomes; inflammation; mesenchymal stem cells.

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