Nephroprotective Efficacy of Echinops spinosus against a Glycerol-Induced Acute Kidney Injury Model

Sara Rizk; Ahmed Esmat Abdel Moneim; Rewaida A Abdel-Gaber; Mohammed I Alquraishi; Simeon Santourlidis; Mohamed A Dkhil

doi:10.1021/acsomega.3c06792

Nephroprotective Efficacy of Echinops spinosus against a Glycerol-Induced Acute Kidney Injury Model

ACS Omega. 2023 Oct 23;8(44):41865-41875. doi: 10.1021/acsomega.3c06792. eCollection 2023 Nov 7.

Authors

Sara Rizk¹, Ahmed Esmat Abdel Moneim², Rewaida A Abdel-Gaber³, Mohammed I Alquraishi⁴, Simeon Santourlidis⁵, Mohamed A Dkhil^{2

6}

Affiliations

¹ Department of Biochemistry and Molecular Biology, Faculty of Pharmacy, Helwan University, Cairo 4034572, Egypt.
² Department of Zoology and Entomology, Faculty of Science, Helwan University, Cairo 4034572, Egypt.
³ Department of Zoology, Faculty of Science, Cairo University, Cairo 3725005, Egypt.
⁴ Department of Community Health Sciences, College of Applied Medical Sciences, King Saud University, Riyadh 11451, Saudi Arabia.
⁵ Epigenetics Core Laboratory, Institute of Transplantation Diagnostics and Cell Therapeutics, Heinrich-Heine-University, Duesseldorf 40225, Germany.
⁶ Applied Science Research Center, Applied Science Private University, Amman 11937, Jordan.

Abstract

Nephroprotection or renal rescue is to revive and restore kidney function after damage, with no need for further dialysis. During acute kidney injury (AKI), sudden and recent reductions in kidney functions occur. Causes are multiple, and prompt intervention can be critical to diminish or prevent morbidity. Echinops spinosus (ES) is a curative plant with proven pharmacological and biological effects including anti-inflammatory, antioxidant, and antibacterial competencies. The principal goal of this research is to scrutinize the nephroprotective features of E. spinosa extract (ESE) against glycerol-induced AKI. Male Wistar albino rats were equally divided into five separated groups: negative control rats (vehicle-injected), ESE control rats (ESE-treated rats), positive control rats, glycerol-induced AKI-model rats (single IM injection of 50% glycerol), and 2 groups of diseased rats but pretreated with different concentrations of ESE for 7 days (ESE₁₅₀ + AKI rats and ESE₂₅₀ + AKI rats). Kidney tissues were collected and used for histopathology analysis. The relative kidney weight percentage was assessed. ESE effects were investigated via scanning several biomarkers, such as serum urea and creatinine, as kidney function biomarkers. Lactate dehydrogenase (LDH) and creatine kinase (CK) activities were examined as rhabdomyolysis (RM) indicators. Kidney injury molecule-1 (Kim-1) and neutrophil gelatinase-associated lipocalin (NGAL) were also examined to investigate kidney injury. Enzymatic and nonenzymatic oxidative stress markers were analyzed, namely, superoxide dismutase (SOD), catalase (CAT), glutathione reductase (GR), glutathione peroxidase (GPx), malondialdehyde (MDA), nitric oxide (NO), and reduced glutathione GSH. Proinflammatory cytokine [tumor necrosis factor-α (TNF-α) and interleukin-1 β (IL-1β)] and the renal proapoptotic protein (Bax) and antiapoptotic protein (Bcl-2) levels were evaluated. Statistical analysis for the resulting data revealed that ESE pretreatment turned AKI-induced biological antioxidant levels to an extent comparable to normal results. Furthermore, ESE decreased kidney function markers and RM-related biomarkers (LDH, CK, Kim-1, and NGAL) compared to those in untreated AKI-model rats. ESE treatment dropped the apoptotic renal Bax levels, enhanced antiapoptotic Bcl-2 manufacture, and disallowed the release of IL-1β and TNF-α. This study revealed the protective effect of ESE as therapeutic medicine against AKI-encouraged oxidative stress, inflammation, and apoptosis. It can be effectively used as adjuvant therapy, helping in renal rescue, and for kidney healing in cases with risk factors of AKI.