Skip to main content

ORIGINAL RESEARCH article

Front. Med.
Sec. Ophthalmology
Volume 11 - 2024 | doi: 10.3389/fmed.2024.1524779
This article is part of the Research Topic New Concepts, Advances, and Future Trends in Clinical Research on Eye Diseases View all 11 articles

Asperulosidic Acid Inhibits the PI3K/Akt/NF-κB Pathway to Suppress Endotoxin-Induced Uveitis

Provisionally accepted
Yong Du Yong Du 1Jing Lu Jing Lu 1Lujia Feng Lujia Feng 2Long Zhao Long Zhao 1Ping Wu Ping Wu 1Yuxia He Yuxia He 1Linbin Zhou Linbin Zhou 3Xing Wang Xing Wang 1*Hui Peng Hui Peng 1*
  • 1 Chongqing Key Lab of Ophthalmology, The First Affiliated Hospital of Chongqing Medical University, Chongqing Eye Institute, Chongqing Branch of National Clinical Research Center for Ocular Diseases, Chongqing, China
  • 2 Shenzhen Eye Hospital, Shenzhen, China
  • 3 State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangzhou, Guangdong Province, China

The final, formatted version of the article will be published soon.

    Uveitis, a severe inflammatory disease affecting the uvea, is associated with visual impairment and irreversible blindness. Asperulosidic Acid (ASPA), derived from Hedyotis diffusa, is known for its notable anti-inflammatory and antioxidant characteristics.The present study explored the potential anti-inflammatory effects and the fundamental processes of ASPA by injecting it or a placebo into the vitreous of rats with endotoxin-induced uveitis (EIU). The severity of the disease was assessed using clinical scores obtained through slit lamp examination. The study involved the examination of protein concentrations and cell count in the aqueous humor (AqH), the detection of inflammatory mediators expressed in the retina. We evaluated the expression levels of various proteins, including the tight junction protein ZO-1, the endothelial marker VE-cadherin, and the key inflammatory mediators NF-κB and its phosphorylated form, along with the regulatory proteins IκB-a and IKK in their phosphorylated and non-phosphorylated states. ASPA treatment significantly reduced the clinical score of EIU, including inflammatory leukocyte penetration, protein accumulation, cellulose-like exudates, the expression of ICAM-1, IL-6, MCP-1, and TNF-α in the AqH; and adhesion of leukocytes. The activation of the PI3K/Akt/NF-κB pathway was observed in EIU. Nevertheless, pretreatment with ASPA significantly suppressed the release of ICAM-1, TNF-α, MCP-1, and IL-6. In conclusion, ASPA may play a role in suppressing LPS-induced inflammation by obstructing the activation of the PI3K/Akt/NF-κB signaling pathway.As a result, ASPA has shown the capacity to significantly reduce immune inflammation.

    Keywords: Uveitis, Asperulosidic acid, EIU, Inflammation, NF-κB

    Received: 08 Nov 2024; Accepted: 18 Dec 2024.

    Copyright: © 2024 Du, Lu, Feng, Zhao, Wu, He, Zhou, Wang and Peng. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

    * Correspondence:
    Xing Wang, Chongqing Key Lab of Ophthalmology, The First Affiliated Hospital of Chongqing Medical University, Chongqing Eye Institute, Chongqing Branch of National Clinical Research Center for Ocular Diseases, Chongqing, China
    Hui Peng, Chongqing Key Lab of Ophthalmology, The First Affiliated Hospital of Chongqing Medical University, Chongqing Eye Institute, Chongqing Branch of National Clinical Research Center for Ocular Diseases, Chongqing, China

    Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.