Lycium barbarum Polysaccharides Regulating miR-181/Bcl-2 Decreased Autophagy of Retinal Pigment Epithelium with Oxidative Stress

  • Oxid Med Cell Longev. 2023 Jan 5:2023:9554457. doi: 10.1155/2023/9554457.
Yi-Jing Yang  1  2  3 ,  Ying Wang  1  2 ,  Ying Deng  1  2 ,  Xiao-Qing Liu  1  2 ,  Jing Lu  1  2 ,  Jun Peng  1  2  4 ,  Jie Li  1  3 ,  Ya-Sha Zhou  1  2  3 ,  Hui-An Zhu  1 ,  Bo Li  1  2  4 ,  Yu-Hui Qin  1  2  3 ,  Qing-Hua Peng  1  2  3  4
Affiliations
  • 1. Hunan University of Chinese Medicine, Changsha, 410208 Hunan Province, China.
  • 2. Institute of Ophthalmology and Otolaryngology of Chinese Medicine, Changsha, 410208 Hunan Province, China.
  • 3. Hunan Provincial Key Laboratory for the Prevention and Treatment of Ophthalmology and Otolaryngology Diseases with Chinese Medicine, Changsha, 410208 Hunan Province, China.
  • 4. Department of Ophthalmology, The First Affiliated Hospital of Hunan University of Chinese Medicine, Changsha, 410007 Hunan Province, China.
PMID: 36644575 DOI: 10.1155/2023/9554457
Abstract

Disturbed structure and dysfunction of the retinal pigment epithelium (RPE) lead to degenerative diseases of the retina. Excessive accumulation of Reactive Oxygen Species (ROS) in the RPE is thought to play an important role in RPE dysfunction and degeneration. Autophagy is a generally low-activity degradation process of cellular components that increases significantly when high levels of oxidative stress are present. Agents with antioxidant properties may decrease Autophagy and provide protection against RPE dysfunction and damage caused by ROS. Lycium barbarum polysaccharide (LBP) has been widely studied as an antioxidant and cell-protective agent. Therefore, we designed this study to investigate the effects of LBP, which inhibits miR-181, on Autophagy in retinal pigment epithelium (RPE) with oxidative stress in vitro and in vivo. In the current study, we found that the highly expressed miR-181 downregulated the expression of Bcl-2 in hydrogen peroxide- (H2O2-) induced ARPE-19 cells, resulting in an increase in ROS, Apoptosis, and Autophagy flux. LBP inhibited the expression of miR-181, decreased the levels of ROS, Apoptosis, and Autophagy flux, and increased cell viability in H2O2-induced ARPE-19 cells, suggesting that LBP provides protection against oxidative damage in ARPE-19 cells. We also found that LBP decreased RPE atrophy and Autophagy flux in rd10 mice. Taken together, the results showed that LBP has a protective effect for RPE under oxidative stress by inhibiting miR-181 and affecting the Bcl-2/Beclin1 Autophagy signaling pathway.

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