The prophylactic anti-aging effect of aspirin (acetylsalicylic acid) on oxidative stress-induced damage in the buccal mucosa of D-galactose-induced aged rats

Abstract

Most living organisms experience time-dependent functional deterioration as they age. To combat aging, aspirin was proposed as an already well-studied drug. However, its antiaging effect is neither well studied nor understood. So, this study intended to assess the proposed antiaging effect of aspirin. Three groups of seven adult male albino rats were established. The control group received saline, the aging model group got a daily single D-galactose subcutaneous injection (300 mg/kg), and the aspirin group consisted of D-galactose-induced aged rats that received a daily aspirin oral dose (60 mg/kg). Drugs were given for 8 weeks. Then, malondialdehyde (MDA) blood level was evaluated, and rats were euthanized. Buccal mucosa samples were obtained for inducible nitric oxide synthase (iNOS) gene expression, histopathological, ultrastructural, and comet analyses. MDA blood level, iNOS gene expression and DNA damage examined by comet assay displayed a significant reduction in the aspirin group when compared to the aging model group. Histopathological and ultrastructural results showed that aspirin ameliorated most of the degenerative signs caused by D-galactose. Thus, it was deduced that aspirin had promising results as an antiaging pharmaceutical agent. However, more studies are needed regarding its translation to human trials.

Keywords: Antiaging; Aspirin; Buccal mucosa; Comet assay; iNOS.

Fig. 1

A bar chart representing mean ± SD of MDA level. # indicates significant difference versus control group. * indicates significant difference versus aging model group. One way ANOVA at p value < 0.05.

Fig. 2

A bar chart representing mean ± SD of iNOS mRNA gene expression. # indicates significant difference versus control group. * indicates significant difference versus aging model group. One way ANOVA at p value < 0.05.

Fig. 3

A photomicrograph of the buccal mucosa. a & d: control group, b & e: aging model group, c & f: aspirin group. (k) keratin layer, (Ep) epithelium, (Lp) lamina propria, (Sm) submucosa, (b) basal cell layer, (p) prickle cell layer, (g) granular cell layer, (pa) papillary layer, (r) reticular layer, white arrows: keratohyaline granules, brown arrows: vacuoles, black arrows: inflammatory cells, asterisk: connective tissue fibers [H&E, a-c: ×100 & d-f: ×400].

Fig. 4

An electron micrograph of the control group’s buccal mucosa showing a: basal cells, b: prickle cells & c: granular cells. (N) nucleus, (n) nucleolus, (asterisk) intercellular spaces, (white arrows) desmosomes, (black arrow) keratohyaline granules. [Magnifications: ×5000, ×8000 & ×5000, respectively].

Fig. 5

An electron micrograph of the aging model group’s buccal mucosa showing a & b: basal cells. a: showing increased intercellular spacing. b: showing atypical nuclear morphology. c: prickle cells. d: granular cells. (N) nucleus, (n) nucleolus, (yellow arrows) vacuoles, (asterisks) intercellular spaces, (white arrow) desmosomes. [Magnifications: ×3000, ×12000, ×12000 & ×5000, respectively].

Fig. 6

An electron micrograph of the aspirin group’s buccal mucosa showing a: basal cells. b: prickle cells. c: granular cells. (N) nucleus, (n) nucleolus, (yellow arrows) vacuoles, (asterisks) intercellular spaces, (white arrow) desmosomes, (black arrows) keratohyaline granules. [Magnifications: ×4000, ×6000 &×1500, respectively].

Fig. 7

(Ι) DNA damage detected by comet assay. (a) control group; (b) aging model group; (c) aspirin group. (ΙΙ) A bar chart representing the mean ± SD of tail DNA%. # indicates significant difference versus control group. * indicates significant difference versus aging model group. One way ANOVA at p value < 0.05.