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

Abstract

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.

Formulation and Evaluation of SNEDDS Loaded with Original Lipophenol for the Oral Route to Prevent Dry AMD and Stragardt’s Disease

“…For example, lutein orally administered at 25 mg/kg/day with corn oil demonstrated its efficacy for protecting photoreceptors for 30 days, with 1.5 h/day (1500 Lux) of light exposure after pretreatment on rats [ 57 ]. In another study, the authors administered Cistanche Tubulosa orally to rats at a rate of 100 mg/kg/day for 74 days, induced degeneration with blue light (150 Lux) 3 h/day during the last 60 days, and demonstrated the protective effect of Cistanche Tubulosa in vivo [ 58 ]. These studies showed that orally administrated antioxidant compounds can have a beneficial effect in the treatment of AMD; however, it would be interesting to study the effects of these compounds over longer exposure times to better imitate the pathophysiological conditions of AMD.…”

Anti-Candidal Activity of the Parasitic Plant Orobanche crenata Forssk

“…Furthermore, this result is consistent with the UPLC-Ms/Ms analysis, which substantially confirmed the presence of several phenolic compounds ( Table 5 ). Interestingly, previously published papers demonstrated an anti-candidal, anti-biofilm, anti-hyphal forming, and cytoprotective effect on retinal cells of some of the UPLC-detected molecules, including acteoside [ 37 , 38 , 39 , 40 , 41 , 42 ], apigenin [ 43 , 44 , 45 , 46 , 47 , 48 , 49 ], luteolin [ 46 , 50 , 51 , 52 , 53 , 54 ], and salidroside [ 55 , 56 , 57 , 58 ]. Since all these biological activities reflect the obtained results, it is possible to hypothesize that the antifungal and re-epithelizing effects of OCLE could be mediated by these chemical agents.…”

Antioxidants and Mechanistic Insights for Managing Dry Age-Related Macular Degeneration

“…Cistanche tubulosa (Schrenk) Hook is an important Chinese traditional medicinal plant, which imparts a wide spectrum of biological activity including antioxidant, neuroprotection, anti-aging, and anti-inflammation primarily due to phenylethanoid glycosides. C. tubulosa extract suppressed apoptosis in blue light-induced retinal degeneration by decreasing the expression of caspase 3 and inhibiting the phosphorylation of c-JNK, p38, and ERK1/2 [303]. It has been conclusively shown that different plant extracts have shown increased promise to combat oxidative stress and its implications to revert AMD pathogenesis, which needs to be validated with further clinical studies.…”