Potential Protective Role of Rutin and Alpha-lipoic Acid Against Cisplatin-induced Nephrotoxicity in Rats

Zaazaa, Asmaa M; Motelp, Bosy Azmy Abd El; Aniss, Nadia Noble-Daoud

doi:10.3923/pjbs.2019.361.371

Cited by 7 publications

(4 citation statements)

References 56 publications

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“…The positively charged species of CP (their active forms) have a great affinity for thiol groups [ 20 , 22 , 25 , 78 , 79 ] and consequently, there is an alteration in the activity of enzymes related to GSH metabolism [ 19 , 26 , 78 ]. In addition, the decrease in GSH could be associated with the formation of disulfide bonds among misfolded proteins in a coupled reaction with the protein disulfide isomerase and ER oxidoreductase 1 [ 73 , 80 , 81 , 82 , 83 ].…”

Section: Discussionmentioning

confidence: 99%

Isoliquiritigenin Pretreatment Induces Endoplasmic Reticulum Stress-Mediated Hormesis and Attenuates Cisplatin-Induced Oxidative Stress and Damage in LLC-PK1 Cells

et al. 2020

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Isoliquiritigenin (IsoLQ) is a flavonoid with antioxidant properties and inducer of endoplasmic reticulum (ER) stress. In vitro and in vivo studies show that ER stress-mediated hormesis is cytoprotective; therefore, natural antioxidants and ER stress inducers have been used to prevent renal injury. Oxidative stress and ER stress are some of the mechanisms of damage involved in cisplatin (CP)-induced nephrotoxicity. This study aims to explore whether IsoLQ pretreatment induces ER stress and produces hormesis to protect against CP-induced nephrotoxicity in Lilly Laboratories Cell-Porcine Kidney 1 (LLC-PK1) cells. During the first stage of this study, both IsoLQ protective concentration and pretreatment time against CP-induced toxicity were determined by cell viability. At the second stage, the effect of IsoLQ pretreatment on cell viability, ER stress, and oxidative stress were evaluated. IsoLQ pretreatment in CP-treated cells induces expression of glucose-related proteins 78 and 94 kDa (GRP78 and GRP94, respectively), attenuates CP-induced cell death, decreases reactive oxygen species (ROS) production, and prevents the decrease in glutathione/glutathione disulfide (GSH/GSSG) ratio, free thiols levels, and glutathione reductase (GR) activity. These data suggest that IsoLQ pretreatment has a moderately protective effect on CP-induced toxicity in LLC-PK1 cells, through ER stress-mediated hormesis, as well as by the antioxidant properties of IsoLQ.

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Section: Discussionmentioning

confidence: 99%

Isoliquiritigenin Pretreatment Induces Endoplasmic Reticulum Stress-Mediated Hormesis and Attenuates Cisplatin-Induced Oxidative Stress and Damage in LLC-PK1 Cells

et al. 2020

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“…Rutin together with alpha-lipoic acid showed the protective effects on cisplatin-induced renal damages in rats. (Zaazaa, El-Motelp, & Aniss, 2019). Treatment with rutin decreased intracellular ROS and malonic dialdehyde and prevented cell apoptosis in human mesangial cells (HMCs).…”

Section: Protective Effect Of Rutin Against Chemotherapy-induced Toxicitymentioning

confidence: 99%

Molecular mechanisms of anticancer effect of rutin

Imani

Maleki

Bohlouli

et al. 2020

Phytotherapy Research

131

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Because of the extensive biological functions of natural substances such as bioflavonoids, and their high safety and low costs, they could have high priority application in the health care system. The antioxidant properties of rutin, a polyphenolic bioflavonoid, have been well documented and demonstrated a wide range of pharmacological applications in cancer research. Since chemotherapeutic drugs have a wide range of side effects and rutin is a safe anticancer agent with minor side effects so recent investigations are performed for study of mechanisms of its anticancer effect.Both in-vivo and in-vitro examinations on anticancer mechanisms of this natural agent have been widely carried out. Regulation of different cellular signaling pathways such as Wnt/β-catenin, p53-independent pathway, PI3K/Akt, JAK/STAT, MAPK, p53, apoptosis as well as NF-ĸB signaling pathways helps to mediate the anticancer impacts of this agent. This study tried to review the molecular mechanisms of rutin anticancer effect on various types of cancer. Deep exploration of these anticancer mechanisms can facilitate the development of this beneficial compound for its application in the treatment of different cancers.

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“…ALA is a naturally occurring dithiol compound [ 22 ]. It is a cofactor for α-ketoglutarate dehydrogenase, branched-chain amino acid dehydrogenase, and pyruvate dehydrogenase [ 23 , 24 , 25 ] ( Figure 2 ). Therefore, ALA is an energy modulator [ 26 , 27 ] ( Figure 3 ).…”

Section: Alpha-lipoic Acidmentioning

confidence: 99%

“…Kidney disorders can be induced by a number of insults, such as diabetes, ischemic reperfusion, drug toxicity, contrast media, and medications [ 7 ]. If not controlled, AKI can lead to renal failure with a 20% mortality rate [ 25 ]. AKI is characterized by an increase in serum creatinine, oliguria, and the presence of kidney damage markers such as albuminuria, electrolyte abnormalities due to tubular disorders, or structural damage seen in imaging or histology [ 9 ].…”

Section: Protective Roles Of α-Lipoic Acid (Ala) In Kidney Injurymentioning

confidence: 99%

Renal-Protective Roles of Lipoic Acid in Kidney Disease

Kamt

Liu

2023

Nutrients

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The kidney is a crucial organ that eliminates metabolic waste and reabsorbs nutritious elements. It also participates in the regulation of blood pressure, maintenance of electrolyte balance and blood pH homeostasis, as well as erythropoiesis and vitamin D maturation. Due to such a heavy workload, the kidney is an energy-demanding organ and is constantly exposed to endogenous and exogenous insults, leading to the development of either acute kidney injury (AKI) or chronic kidney disease (CKD). Nevertheless, there are no therapeutic managements to treat AKI or CKD effectively. Therefore, novel therapeutic approaches for fighting kidney injury are urgently needed. This review article discusses the role of α-lipoic acid (ALA) in preventing and treating kidney diseases. We focus on various animal models of kidney injury by which the underlying renoprotective mechanisms of ALA have been unraveled. The animal models covered include diabetic nephropathy, sepsis-induced kidney injury, renal ischemic injury, unilateral ureteral obstruction, and kidney injuries induced by folic acid and metals such as cisplatin, cadmium, and iron. We highlight the common mechanisms of ALA’s renal protective actions that include decreasing oxidative damage, increasing antioxidant capacities, counteracting inflammation, mitigating renal fibrosis, and attenuating nephron cell death. It is by these mechanisms that ALA achieves its biological function of alleviating kidney injury and improving kidney function. Nevertheless, we also point out that more comprehensive, preclinical, and clinical studies will be needed to make ALA a better therapeutic agent for targeting kidney disorders.

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Potential Protective Role of Rutin and Alpha-lipoic Acid Against Cisplatin-induced Nephrotoxicity in Rats

Cited by 7 publications

References 56 publications

Isoliquiritigenin Pretreatment Induces Endoplasmic Reticulum Stress-Mediated Hormesis and Attenuates Cisplatin-Induced Oxidative Stress and Damage in LLC-PK1 Cells

Isoliquiritigenin Pretreatment Induces Endoplasmic Reticulum Stress-Mediated Hormesis and Attenuates Cisplatin-Induced Oxidative Stress and Damage in LLC-PK1 Cells

Molecular mechanisms of anticancer effect of rutin

Renal-Protective Roles of Lipoic Acid in Kidney Disease

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