article · International Journal of Molecular Sciences
Aging is linked to progressive oxidative stress, which causes cellular damage over time. This investigation assessed whether oral supplementation with quercetin, a natural bioactive compound, protects against chemically induced aging-related damage in the pancreas and kidneys of male rats. Laboratory rats received daily D-galactose injections to induce oxidative aging changes alongside oral doses of quercetin at 25, 50, or 100 milligrams per kilogram of body weight for 42 days. D-galactose exposure led to harmful changes across pancreatic and renal tissues, increasing markers of aging, inflammation, and programmed cell death while reducing antioxidant defences and tissue function. Oral quercetin treatment countered these damaging effects in a dose-dependent manner by lowering inflammatory and apoptotic indicators and restoring functional and antioxidant markers, indicating potential benefits for mitigating age-related decline.
Aging tissues frequently suffer from chronic inflammation and oxidative damage, leading to organ decline, particularly in the kidneys and pancreas. Identifying accessible, naturally derived compounds that can mitigate these internal stresses offers a potential pathway for preventative health strategies. This research provides biological evidence in animal models that dietary antioxidants such as quercetin could help slow tissue-level degradation associated with the natural aging process.
This research points to potential applications in dietary supplements, nutraceuticals, and functional health formulations targeting age-related renal and metabolic decline. Likely end users include nutraceutical companies and consumer wellness brands. However, this is early-stage animal research, and significant formulation work, validation in higher models, and human clinical trials are necessary before any commercial preventive health claims or products can be developed.
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Aging is an oxidative stress-associated process that progresses with age. Our aim is to delay or attenuate these oxidative alterations and to keep individuals healthy as they age using natural compounds supplementation. Therefore, we conducted the present study to investigate the protective potentials of quercetin against D-galactose (D-gal)-associated oxidative alterations that were induced experimentally in male Wistar rats. Forty-five rats were randomly allocated into five groups of nine rats each. The groups were a control group that was reared on a basal diet and injected subcutaneously with 120 mg D-gal dissolved in physiological saline solution (0.9% NaCl) per kg body weight daily and quercetin-treated groups that received the same basal diet and subcutaneous daily D-gal injections were supplemented orally with 25, 50, and 100 mg of quercetin per kg body weight for 42 days. Pancreatic and renal samples were subjected to histopathological, immunohistochemical, and relative mRNA expression assessments. Aging (<i>p53</i>, <i>p21</i>, <i>IL-6</i>, and <i>IL-8</i>), apoptotic (<i>Bax</i>, <i>CASP-3</i>, and caspase-3 protein), proliferative (Ki67 protein), antiapoptotic (<i>Bcl2</i> and Bcl2 protein), inflammatory (<i>NF-κB</i>, <i>IL-1β</i>, and <i>TNF-α</i>), antioxidant (<i>SOD1</i>), and functional markers (<i>GCLC</i> and <i>GCLM</i> genes and insulin, glucagon, and podocin proteins) were determined to evaluate the oxidative alterations induced by D-gal and the protective role of quercetin. D-gal caused oxidative alterations of the pancreas and kidneys observed via upregulations of aging, apoptotic, and inflammatory markers and downregulated the antiapoptotic, proliferative, antioxidant, and functional markers. Quercetin potentially attenuated these aging-related oxidative alterations in a dose-dependent manner. Finally, we can conclude that quercetin supplementation is considered as a promising natural protective compound that could be used to delay the aging process and to maintain human health.
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DOI: 10.3390/ijms21124348
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