Abstract
KIOM-79 is an herbal mixture of parched Puerariae radix, gingered Magnoliae cortex, Glycyrrhizae radix and Euphorbiae radix. In the present study, we determined the efficacy and possible mechanism of KIOM-79 on the advanced glycation end product (AGE)-modified bovine serum albumin (BSA)-induced apoptosis of cultured bovine retinal pericytes and rat retinal pericytes in Zucker diabetic fatty (ZDF) rats. Seven-week-old male ZDF rats were treated with KIOM-79 (50 mg/kg body weight) once a day orally for 13 weeks. KIOM-79 significantly inhibited pericyte apoptosis which were induced by the AGE-BSA treatment. The KIOM-79 treatment markedly suppressed the activation of nuclear factor-kappaB (NF-κB) through the inhibition of inhibitory κB kinase complex. In addition, the oral administration of KIOM-79 inhibited the changes in retinal vasculature (vascular hyperpermeability, acellular capillary). KIOM-79 strongly inhibited pericyte apoptosis, NF-κB activation and the expression of pro-apoptotic Bax and tumor necrosis factor-α. Our results suggest that KIOM-79 may exert inhibitory effects on AGE-induced pericyte apoptosis by blocking NF-κB activation, thereby ameliorating retinal microvascular dysfunction.
Highlights
Retinal microvascular cells undergo functional alterations and cell death under diabetic conditions [1,2,3]
Korea Institute of Oriental Medicine (KIOM)-79 Inhibits Pericyte Apoptosis Induced by advanced glycation end product (AGE)-BSA The retinal pericyte apoptosis induced by AGE-modified bovine serum albumin (BSA) was examined in the presence of various concentrations of AGE-BSA (0, 10, 50, 100 and 200 mg/mL) for 6 hours (Fig. 2A)
To observe the effects of KIOM-79 on AGE-BSA-induced pericyte apoptosis, various concentrations of KIOM-79 (1, 5 and 10 mg/mL) were added 1 hour before the pericytes were stimulated for 6 hours with 100 mg/mL AGE-BSA
Summary
Retinal microvascular cells undergo functional alterations and cell death under diabetic conditions [1,2,3]. Advanced glycation end products (AGEs) are the late products of non-enzymatic glycation. The levels of these products are much higher in patients with diabetes [4]. Administration of exogenous AGEs to non-diabetic animals induced thickening of the basement membrane of the retinal vessels [8], increased leukocyte adhesion [9] and increased breakdown of the blood retinal barrier [10]. It was reported that AGEs are directly linked with the apoptotic cell death of retinal pericytes [1,11,12]. It was found that enhanced apoptosis of the retinal pericyte is associated with nuclear factor (NF)-kB [16,17]. NF-kB activation due to hyperglycemia induces accelerated pericyte loss [16]
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