Osteomeles schwerinae Extract and Its Major Compounds Inhibit Methylglyoxal-Induced Apoptosis in Human Retinal Pigment Epithelial Cells

Abstract

The accumulation and formation of advanced glycation end products (AGEs) are related to diabetes and age-related disease. Osteomeles schwerinae C. K. Schneid. (Rosaceae, OSSC) is used traditionally for the treatment of various diseases in Asia. Previous studies have shown that OSSC elicits preventive effects in an in vivo model of diabetes. This study was to evaluate the antiapoptotic effects of dried leaves and twigs of OSSC extract and its major compounds in ARPE-19 cells—spontaneously arising human retinal pigment epithelial cells—under diabetic conditions. To examine the effects of an OSSC extract and its active compounds (acetylvitexin, hyperoside and quercitrin) on apoptosis in methylglyoxal (MG, the active precursor in the formation of AGEs)-treated ARPE-19 cells and the mechanism by which these effects occur, apoptosis was measured using flow cytometry analysis. Protein expression levels of phospho-p53 (p-p53), Bax and Bcl-2 were determined by western blot analyses. The OSSC extract inhibited apoptosis in MG-treated ARPE-19 cells in a dose-dependent manner. The major compounds also reduced the rate of apoptosis. Both the extract and major compounds also inhibited the expression of p-p53 and Bax and increased the levels of Bcl-2 that had been previously reduced by MG treatment. The OSSC extract (0.1 μg/mL) and its major compounds (0.01 μM) attenuated apoptosis in ARPE-19 cells under toxic diabetic conditions by downregulating of expression of p-p53 and Bax. OSSC may serve as an alternative therapy to retard the development of diabetic retinopathy.

Alu antisense RNA ameliorates methylglyoxal-induced human lens epithelial cell apoptosis by enhancing antioxidant defense

“…Depletion of GSH suppresses the Glo1 function and induces significant MGO accumulation [54] . Several reports have proved that MGO induces apoptosis in cells, including HK-2 cells [55] , rat INS-1 pancreatic β-cells [56] and human retinal pigment epithelial cells [57] . Our results confirmed that MGO can also induce apoptosis in HLECs.…”

Proanthocyanidins attenuate the high glucose‐induced damage of retinal pigment epithelial cells by attenuating oxidative stress and inhibiting activation of the NLRP3 inflammasome

“…Although the underlying mechanisms have not been completely uncovered, advanced glycation end‐products (AGEs) and reactive oxygen species (ROS) have been demonstrated to be closely associated with the pathogenesis of DR. [ 2–4 ] Production of ROS and AGEs has been reported to lead to oxidative stress and inflammatory responses via multiple cellular signaling pathways, thereby inducing injury of the retina. [ 5–7 ] A recent study confirmed that the loss of pericyte selection was an important early event in the pathogenesis of DR. Accumulation of AGEs in the pericytes can trigger the production of ROS, in turn inducing activation of caspase‐3 that initiates the apoptosis process.…”

The Herbal Combination CPA4-1 Inhibits Changes in Retinal Capillaries and Reduction of Retinal Occludin in db/db Mice

“…Aster koraiensis extract prevents retinal pericyte apoptosis in streptozotocin (STZ)-induced diabetic rats [ 13 ]. Osteomeles schweinae extract inhibits methylglyoxal (an active precursor in the formation of AGEs)-induced apoptosis in human retinal pigment epithelial cells [ 14 ]. Cinnamomi Ramulus (the twig of Cinnamomum cassia Blume; Lauraceae) and Paeoniae Radix (the root of Paeonia lactiflora Pallas; Paeoniaceae) have been shown to exert efficacy in inhibiting the formation of AGEs in our previous study.…”