The importance of natural chalcones in ischemic organ damage: Comprehensive and bioinformatic analysis review

Abstract

Over the last few decades, extensive research has been conducted, yielding a detailed account of thousands of newly discovered compounds of natural origin and their biological activities, all of which have the potential to be used for a wide range of therapeutic purposes. There are multiple research papers denoting the central objective of chalcones, which have been shown to have therapeutic potential against various forms of ischemia. The various aspects of chalcones are discussed in this review regarding molecular mechanisms involved in the promising anti‐ischemic potential of these chalcones. The main mechanisms involved in these protective effects are Nrf2/Akt activation and NF‐κB/TLR4 suppression. Furthermore, in‐silico studies were carried out to discover the probable binding of these chalcones to Keap‐1 (an inhibitor of Nrf2), Akt, NF‐κB, and TLR4 protein molecules. Besides, network pharmacology analysis was conducted to predict the interacting partners of these signals. The obtained results indicated that Nrf2, Akt, NF‐κB, and TLR4 are involved in the beneficial anti‐ischemic actions of chalcones. Conclusively, the present findings show that chalcones as anti‐ischemic agents have a valid rationale. The discussed studies will provide a comprehensive viewpoint on chalcones and can help to optimize their effects in different ischemia. Practical applications Ischemic organ damage is an unavoidable pathological condition with a high worldwide incidence. According to the current research progress, natural chalcones have been proved to treat and/or prevent various types of ischemic organ damage by alleviating oxidative stress, inflammation, and apoptosis by different molecular mechanisms. This article displays the comprehensive research progress and the molecular basis of ischemic organ damage pathophysiology and introduces natural chalcones' mechanism in the ischemic organ condition.

Cardamonin mitigates kidney injury by modulating inflammation, oxidative stress, and apoptotic signaling in rats subjected to renal ischemia and reperfusion

“…Twenty Sprague Dawley rats (200-350 g, aged 20-24 weeks) were randomly divided into four groups (n=5 each): the sham group received anesthesia and underwent only abdominal opening; the control group underwent anesthesia, abdominal incision, and renal ischemia induced by clamping the renal arteries for 30 minutes followed by 2 hours of reperfusion [ 13 , 14 ]; the vehicle-treated group received the cardamonin vehicle intraperitoneally (i.p.) (10% DMSO, 40% PEG300, 5% Tween 80, and 45% normal saline) 30 minutes before ischemia; the cardamonin group received 5 mg/kg of cardamonin i.p.…”