New Therapeutic Concept of NAD Redox Balance for Cisplatin Nephrotoxicity

Oh, Gi‐Su; Kim, Hyungjin; Shen, AiHua; Lee, Su-Bin; Yang, Sei‐Hoon; Shim, Hyeok; Cho, Eun Young; Kwon, Kang‐Beom; Kwak, Tae Hwan; So, Hong-Seob

doi:10.1155/2016/4048390

Cited by 40 publications

(37 citation statements)

References 116 publications

(148 reference statements)

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“…NF-κB can mediate inflammatory response, by affecting the expression of a large number of proinflammatory mediators such as TNF-α, COX-2 and inducible nitric oxide [35]. Cisplatininduced ROS production activates NF-B, which in turn induces the production of proinflammatory cytokines [36]. In the current study, the cisplatin-treated group showed a pro-inflammatory response as evidenced by significant increase in NF-kB expression.…”

Section: Discussionmentioning

confidence: 51%

Piceatannol Ameliorates Cisplatin-Induced Histological and Biochemical Alterations in Rats Kidney

Wahdan

Azab

Elsherbiny

et al. 2017

Int J Pharm Pharm Sci

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Objective: The present study was designed to investigate the effect of different doses of piceatannol (PIC) on cisplatin-induced biochemical and histological alterations in rat kidney. Methods:Male Wistar rats received a single intraperitoneal (i. p.) injection of cisplatin (7 mg/kg). PIC was given in different daily doses (5, 10 and 20 mg/kg) i. p., for seven days, starting two days before cisplatin injection. Nephrotoxicity was evaluated by means of measurement of blood urea nitrogen (BUN), serum creatinine and histopathological examination of the kidney. We also investigated the antioxidant effect of the most effective dose of PIC by measuring reduced glutathione (GSH) and lipid peroxides levels. Moreover, the ability of PIC to affect nuclear factor kappa B (NF-kB) expression was determined by immunohistochemical analysis. Results:A single dose of cisplatin (7 mg/kg) significantly increased BUN and creatinine levels, as well as relative kidney weight, compared to the control group. In addition, significant histopathological alterations including tubular necrosis, hemorrhage and casts formation were observed. PIC was given in different doses (5, 10 and 20 mg/kg) for 7 d, starting 2 d before cisplatin injection. PIC dose 10 mg/kg was the most effective in preventing these alterations. PIC significantly increased GSH level and decreased lipids peroxidation compared to cisplatin group. Moreover, PIC significantly mitigated cisplatin-induced expression of NF-kB.Conclusion: PIC has the potential to ameliorate cisplatin-induced renal injury.

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Section: Discussionmentioning

confidence: 51%

Piceatannol Ameliorates Cisplatin-Induced Histological and Biochemical Alterations in Rats Kidney

Wahdan

Azab

Elsherbiny

et al. 2017

Int J Pharm Pharm Sci

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“…The Nox family consists of seven members (Noxs 1–5, Duox1 and 2). Nox2 and Nox4 are highly expressed within the kidney and Nox4 is known as the predominant form, which plays important roles in renal oxidative stress and kidney injury (Gill and Wilcox, 2006; Sedeek et al, 2013; Kim et al, 2016; Oh et al, 2016). Our data show that lentivirus-mediated knockdown of Nox4 in vivo significantly attenuated cisplatin nephropathy.…”

Section: Discussionmentioning

confidence: 99%

Protocatechuic Aldehyde Attenuates Cisplatin-Induced Acute Kidney Injury by Suppressing Nox-Mediated Oxidative Stress and Renal Inflammation

et al. 2016

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Cisplatin is a classic chemotherapeutic agent widely used to treat different types of cancers including ovarian, head and neck, testicular and uterine cervical carcinomas. However, cisplatin induces acute kidney injury by directly triggering an excessive inflammatory response, oxidative stress, and programmed cell death of renal tubular epithelial cells, all of which lead to high mortality rates in patients. In this study, we examined the protective effect of protocatechuic aldehyde (PA) in vitro in cisplatin-treated tubular epithelial cells and in vivo in cisplatin nephropathy. PA is a monomer of Traditional Chinese Medicine isolated from the root of S. miltiorrhiza (Lamiaceae). Results show that PA prevented cisplatin-induced decline of renal function and histological damage, which was confirmed by attenuation of KIM1 in both mRNA and protein levels. Moreover, PA reduced renal inflammation by suppressing oxidative stress and programmed cell death in response to cisplatin, which was further evidenced by in vitro data. Of note, PA suppressed NAPDH oxidases, including Nox2 and Nox4, in a dosage-dependent manner. Moreover, silencing Nox4, but not Nox2, removed the inhibitory effect of PA on cisplatin-induced renal injury, indicating that Nox4 may play a pivotal role in mediating the protective effect of PA in cisplatin-induced acute kidney injury. Collectively, our data indicate that PA blocks cisplatin-induced acute kidney injury by suppressing Nox-mediated oxidative stress and renal inflammation without compromising anti-tumor activity of cisplatin. These findings suggest that PA and its derivatives may serve as potential protective agents for cancer patients receiving cisplatin treatment.

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“…Oxidative damage is one of the important pathogeneses by which cisplatin triggers kidney tissue injury [27]. In mice kidney tissues, cisplatin significantly increased oxidative stress marker 3-NT expression (Figure 4(a)) and inhibited antioxidant enzyme activities, including T-SOD and GSH-Px (Figures 4(b) and 4(c)), compared with the control group.…”

Section: Aps Attenuates Cisplatin-induced Oxidative Damage In Mice Kimentioning

confidence: 99%

Astragalus Polysaccharide Attenuates Cisplatin-Induced Acute Kidney Injury by Suppressing Oxidative Damage and Mitochondrial Dysfunction

Tang

et al. 2020

BioMed Research International

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Cisplatin is a widely used chemotherapeutic drug in the treatment of various solid tumors. However, the cisplatin-induced acute kidney injury remains a disturbing complication, which still lacks effective prevention. Cisplatin-induced oxidative damage and mitochondrial dysfunction are anticipated to be crucial in the occurrence of kidney injury. Astragalus polysaccharide (APS) has been reported to possess multiple biological activities including anti-inflammatory, antioxidant, and mitochondria protection. In this study, we investigated the potentially protective effect of APS against cisplatin-induced kidney injury both in vivo and in vitro. We found that APS pretreatment attenuated the cisplatin-induced renal dysfunction and histopathological damage in mice; in addition, it also protected the viability of HK-2 cells upon cisplatin exposure. APS attenuated the cisplatin-induced oxidative damage by reducing reactive oxygen species (ROS) generation and recovering the activities of total superoxide dismutase and glutathione peroxidase in mice kidney. In addition, electron microscope analysis indicated that cisplatin induced extensive mitochondrial vacuolization in mice kidney. However, APS administration reversed these mitochondrial morphology changes. In HK-2 cells, APS reduced the cisplatin-induced mitochondrial and intracellular ROS generation. Furthermore, APS protected the normal morphology of mitochondria, blocked the cisplatin-induced mitochondrial permeability transition pore opening, and reduced the cytochrome c leakage. Subsequently, APS reduced the cisplatin-induced apoptosis in mice renal and HK-2 cells. In conclusion, our data suggested that APS pretreatment might prevent cisplatin-induced kidney injury through attenuating oxidative damage, protecting mitochondria, and ameliorating mitochondrial-mediated apoptosis.

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New Therapeutic Concept of NAD Redox Balance for Cisplatin Nephrotoxicity

Cited by 40 publications

References 116 publications

Piceatannol Ameliorates Cisplatin-Induced Histological and Biochemical Alterations in Rats Kidney

Piceatannol Ameliorates Cisplatin-Induced Histological and Biochemical Alterations in Rats Kidney

Protocatechuic Aldehyde Attenuates Cisplatin-Induced Acute Kidney Injury by Suppressing Nox-Mediated Oxidative Stress and Renal Inflammation

Astragalus Polysaccharide Attenuates Cisplatin-Induced Acute Kidney Injury by Suppressing Oxidative Damage and Mitochondrial Dysfunction

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