Lycium barbarum glycopeptide (wolfberry extract) slows N-methyl-N-nitrosourea-induced degradation of photoreceptors

Author:

Kong Qihang12,Han Xiu3,Cheng Haiyang3,Liu Jiayu2,Zhang Huijun24,Dong Tangrong5,Chen Jiansu16,So Kwok-Fai3768,Mi Xuesong26,Xu Ying376,Tang Shibo16

Affiliation:

1. Department of Ophthalmology, Aier Eye Hospital, Jinan University, Guangzhou, Guangdong Province, China

2. Department of Ophthalmology, The First Affiliated Hospital of Jinan University, Guangzhou, Guangdong Province, China

3. Guangdong-Hong Kong-Macau Institute of CNS Regeneration, Key Laboratory of CNS Regeneration (Ministry of Education), Jinan University, Guangzhou, Guangdong Province, China

4. Department of Ophthalmology, Guangzhou Panyu Central Hospital, Guangzhou, Guangdong Province, China

5. School of Stomatology, Jinan University, Guangzhou, Guangdong Province, China

6. Aier Academician Station, Changsha, Hunan Province, China

7. Co-Innovation Center of Neuroregeneration, Nantong University, Nantong, Jiangsu Province, China

8. State Key Laboratory of Brain and Cognitive Sciences, Hong Kong Special Administrative Region, China

Abstract

Abstract Photoreceptor cell degeneration leads to blindness, for which there is currently no effective treatment. Our previous studies have shown that Lycium barbarum (L. barbarum) polysaccharide (LBP) protects degenerated photoreceptors in rd1, a transgenic mouse model of retinitis pigmentosa. L. barbarum glycopeptide (LbGP) is an immunoreactive glycoprotein extracted from LBP. In this study, we investigated the potential protective effect of LbGP on a chemically induced photoreceptor-degenerative mouse model. Wild-type mice received the following: oral administration of LbGP as a protective pre-treatment on days 1–7; intraperitoneal administration of 40 mg/kg N-methyl-N-nitrosourea to induce photoreceptor injury on day 7; and continuation of orally administered LbGP on days 8–14. Treatment with LbGP increased photoreceptor survival and improved the structure of photoreceptors, retinal photoresponse, and visual behaviors of mice with photoreceptor degeneration. LbGP was also found to partially inhibit the activation of microglia in N-methyl-N-nitrosourea-injured retinas and significantly decreased the expression of two pro-inflammatory cytokines. In conclusion, LbGP effectively slowed the rate of photoreceptor degeneration in N-methyl-N-nitrosourea-injured mice, possibly through an anti-inflammatory mechanism, and has potential as a candidate drug for the clinical treatment of photoreceptor degeneration.

Publisher

Medknow

Subject

Developmental Neuroscience

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