Journal of ethnopharmacology · 2026
Lycium barbarum glycopeptide alleviates diabetic retinopathy and hepatic lipid disorder via modulation of the LXR-α/ABC transporter axis.
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Wang Yixin, Zhang Yunqi, Che Xiaoyang, Xu Xiaoyu, Wang Kai, Shi Yahong, Wang Min, Wang Fan, Liu Sai, Jia Zhihao, Luo Yun, Sun Xiaobo
Аннотация
ETHNOPHARMACOLOGICAL RELEVANCE: Lycium barbarum L. (Solanaceae) is traditionally used to safeguard liver function and promote eye health. However, whether its bioactive constituent Lycium barbarum glycopeptide (LbGp) simultaneously exerts beneficial effects on diabetic retinopathy (DR) and associated hepatic metabolic dysfunction remains to be elucidated.
AIM OF THE STUDY: This study aims to investigate the therapeutic effect of LbGp on diabetic liver-eye comorbidity and explore its underlying mechanisms.
MATERIALS AND METHODS: The retinal laminar structure and fundus vasculopathy of early DR mice were observed by optical coherence tomography (OCT) and fundus fluorescein angiography (FFA). The integrity of the blood-retinal barrier (BRB) was evaluated by transmission electron microscopy and immunofluorescence. Hepatic pathological changes were assessed by histological examination, and serum biochemical indices were measured using commercial kits. The potential mechanisms were explored via integrated multi-omics and Western blot analysis.
RESULTS: Early DR in db/db mice was characterized by retinal thinning and mild edematous degeneration. LbGp intervention significantly reduced cellular edema and increased the thickness of the inner nuclear layer (INL) and photoreceptor outer segment (POS) layer to the retinal pigment epithelium (RPE) layer. LbGp restored the expression of tight junctions, Claudin-1, Occludin, and the endothelial cell marker CD31 in the BRB. Furthermore, LbGp ameliorated dyslipidemia, serum cholestasis, and hepatic injury in DR mice. Combined serum metabolomics and liver proteomics analysis revealed that LbGp primarily modulates pathways including fatty acid metabolism, unsaturated fatty acid biosynthesis, and ABC transporters. Mechanistic studies revealed that LbGp modulates cholesterol transport associated with upregulation of LXR-α/ABCA1/ABCG1 expression, while simultaneously enhancing cholesterol conversion through increased CYP7A1/CYP8B1 and ABCG2 expression. This dual action facilitates the production of HDL-C, apoA-I, and pre-β-HDL while reducing LDL-C, FC, and 7-KC deposition.
CONCLUSION: This study shows that LbGp can simultaneously improve early DR and liver metabolic dysfunction in db/db mice. We observed for the first time that LbGp modulated the LXR-α/ABC transporter pathway, suggesting that LXR-α mediated lipid metabolism may be a potential target linked to hepatic-ocular changes in diabetic complications.
AIM OF THE STUDY: This study aims to investigate the therapeutic effect of LbGp on diabetic liver-eye comorbidity and explore its underlying mechanisms.
MATERIALS AND METHODS: The retinal laminar structure and fundus vasculopathy of early DR mice were observed by optical coherence tomography (OCT) and fundus fluorescein angiography (FFA). The integrity of the blood-retinal barrier (BRB) was evaluated by transmission electron microscopy and immunofluorescence. Hepatic pathological changes were assessed by histological examination, and serum biochemical indices were measured using commercial kits. The potential mechanisms were explored via integrated multi-omics and Western blot analysis.
RESULTS: Early DR in db/db mice was characterized by retinal thinning and mild edematous degeneration. LbGp intervention significantly reduced cellular edema and increased the thickness of the inner nuclear layer (INL) and photoreceptor outer segment (POS) layer to the retinal pigment epithelium (RPE) layer. LbGp restored the expression of tight junctions, Claudin-1, Occludin, and the endothelial cell marker CD31 in the BRB. Furthermore, LbGp ameliorated dyslipidemia, serum cholestasis, and hepatic injury in DR mice. Combined serum metabolomics and liver proteomics analysis revealed that LbGp primarily modulates pathways including fatty acid metabolism, unsaturated fatty acid biosynthesis, and ABC transporters. Mechanistic studies revealed that LbGp modulates cholesterol transport associated with upregulation of LXR-α/ABCA1/ABCG1 expression, while simultaneously enhancing cholesterol conversion through increased CYP7A1/CYP8B1 and ABCG2 expression. This dual action facilitates the production of HDL-C, apoA-I, and pre-β-HDL while reducing LDL-C, FC, and 7-KC deposition.
CONCLUSION: This study shows that LbGp can simultaneously improve early DR and liver metabolic dysfunction in db/db mice. We observed for the first time that LbGp modulated the LXR-α/ABC transporter pathway, suggesting that LXR-α mediated lipid metabolism may be a potential target linked to hepatic-ocular changes in diabetic complications.