Novel Protective Effects of Cistanche Tubulosa Extract Against Low-Luminance Blue Light-Induced Degenerative Retinopathy

Autor: Jau-Der Ho, Man Ru Wu, Yu Wen Cheng, George Hsiao, Cheng Hui Lin
Rok vydání: 2018
Předmět:
Male
0301 basic medicine
Retinal degeneration
Cistanche
Light
Physiology
Cistanche tubulosa extract
Administration
Oral

Apoptosis
Retinal Pigment Epithelium
Protective Agents
Retina
lcsh:Physiology
lcsh:Biochemistry
03 medical and health sciences
chemistry.chemical_compound
Western blot
In vivo
medicine
Animals
lcsh:QD415-436
Viability assay
Phosphorylation
Mitogen-Activated Protein Kinase 1
Mitogen-Activated Protein Kinase 3
TUNEL assay
lcsh:QP1-981
medicine.diagnostic_test
Caspase 3
Plant Extracts
Retinal Degeneration
JNK Mitogen-Activated Protein Kinases
Retinal
Hydrogen Peroxide
medicine.disease
Molecular biology
Rats
Staining
Oxidative Stress
Retinal pigment epithelial cells
030104 developmental biology
Proto-Oncogene Proteins c-bcl-2
chemistry
Terminal deoxynucleotidyl transferase
Blue light
Zdroj: Cellular Physiology and Biochemistry, Vol 51, Iss 1, Pp 63-79 (2018)
ISSN: 1421-9778
1015-8987
Popis: Background/Aims: Blue light-emitting diode light (BLL)-induced phototoxicity plays an important role in ocular diseases and causes retinal degeneration and apoptosis in human retinal pigment epithelial (RPE) cells. Cistanche tubulosa extract (CTE) is a traditional Chinese medicine with many beneficial protective properties; however, few studies have examined the ocular protective roles of CTE. In this study, we investigated the mechanisms underlying the effects of CTE on BLL-induced apoptosis in vitro and in vivo. Methods: RPE cells were applied in the current in vitro study and cell viability was determined by an 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. Apoptosis-related protein expression was determined by western blot analysis and immunofluorescence staining. Brown Norway rats were used to examine exposure to commercially available BLL in vivo. Hematoxylin and eosin staining, terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL), and western blot assays were used to examine retinal morphological deformation. Results: CTE significantly inhibited hydrogen peroxide-, tert-butyl hydroperoxide-, sodium azide-, and BLL-induced RPE damage. Further, CTE reduced the expression of apoptotic markers such as cleaved caspase-3 and TUNEL staining after BLL exposure by inactivating apoptotic pathways, as shown via immunofluorescent staining. In addition, CTE inhibited the BLL-induced phosphorylation of c-Jun N-terminal kinase, extra signal-related kinases 1/2, and p38 in RPE cells. In vivo, the oral administration of CTE rescued 60-day periodic BLL exposure-induced decrements in retinal thickness and reduced the number of TUNEL-positive cells in the brown Norway rat model. Conclusion: CTE is a potential prophylactic agent against BLL-induced phototoxicity.
Databáze: OpenAIRE