Preprint Article Version 1 This version is not peer-reviewed

Synthesis and Therapeutic Potential of Urolithin-C on Oxidative Stress Induced Tissue Damage

Version 1 : Received: 23 October 2024 / Approved: 24 October 2024 / Online: 24 October 2024 (17:16:34 CEST)

How to cite: Manjappa, V. K.; Venkatappa, M. M.; Elhindi, K. M.; Sannaningaiah, D. Synthesis and Therapeutic Potential of Urolithin-C on Oxidative Stress Induced Tissue Damage. Preprints 2024, 2024101948. https://doi.org/10.20944/preprints202410.1948.v1 Manjappa, V. K.; Venkatappa, M. M.; Elhindi, K. M.; Sannaningaiah, D. Synthesis and Therapeutic Potential of Urolithin-C on Oxidative Stress Induced Tissue Damage. Preprints 2024, 2024101948. https://doi.org/10.20944/preprints202410.1948.v1

Abstract

Ellagitannins (ETs) are the group of tannins found in fruits, nuts and seeds; they undergo hydrolysis in the human digestive tract to form ellagic acid (EA). EA further converted into various forms of Urolithin derivatives (A, B, C, D, M-5, M-6 and M-7) by gut micro biota. Perhaps, the pharmacological properties of said Urolithins were extensively studied, while, little is known about the therapeutic role of synthetic Urolithin-C on oxidative stress induced eryptosis and tissue damage. Therefore, in the current study we investigated the ameliorative role of chemically syn-thesized Urolithin-C on sodium nitrite and Diclofenac (DFC) induced eryptosis and vital organ damage respectively. Urolithin-C was synthesized using chemical method and characterized by High-Performance Liquid Chromatography (HPLC), Nuclear Magnetic Resonance (NMR), Fourier Transform Infrared Spectroscopy (FTIR), and Liquid Chromatography Mass Spectroscopy (LC-MS). The synthesized Urolithin-C scavenged free radicals (DPPH, H2O2) and reduced ferric iron to ferrous iron, revealed its antioxidant activity. The observed antioxidant potential of Uro-lithin-C was investigated in sodium nitrite induced stress in RBC and Diclofenac induced tissue damage in rats. Interestingly, Urolithin-C normalized the sodium nitrate-induced oxidative stress in red blood cells by regulating stress markers, such as lipid peroxidation (LPO), total thiol (TT), and protein carbonyl content (PCC), and endogenous antioxidant enzymes superoxide dis-mutase (SOD) and catalase (CAT) in a dose dependent manner. Similar effect was also observed in the tissue homogenates of liver, kidney, heart and pancreas taken from the Diclofenac injected Sprague Dawley rats. The tissue sections (liver, kidney, heart and pancreas) obtained from the Diclofenac (DFC) received rats showed massive destruction of hepatocytes, nephrons, cardiocytes and pancreas. However, Urolithin-C received rats tissue sections showed normal histology compared to the positive (Silymarin) control treated groups. In addition, Urolithin-C regulated the key tissue specific biochemical markers in DFC injected Sprague Dawley rats serum strengthened its tissue protective role. In conclusion, chemically synthesized Urolithin-C regulated NaNO2 and diclofenac induced oxidative stress in RBC and vital organs through its antioxidant property.

Keywords

Ellagitannins; Urolithin-C; Oxidative stress; Tissue damage; Antioxidant activity

Subject

Biology and Life Sciences, Life Sciences

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