Tempol (4-hydroxy tempo) protects mice from cisplatin-induced acute kidney injury <i>via</i> modulation of expression of aquaporins and kidney injury molecule-1

Afjal, Mohd Amir; Goswami, Poonam; Ahmad, Shahzad; Dabeer, Sadaf; Akhter, Juheb; Salman, Mohammad; Mangla, Anuradha; Raisuddin, Sheikh

doi:10.1080/01480545.2020.1831011

Cited by 10 publications

(8 citation statements)

References 43 publications

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“…Its expression was not detected in the normal kidney tissue. However, with the injury of proximal tubule epithelial cells KIM-1 expression was found to be upregulated in CP-induced AKI 15 , 45 . In this study we also characterize the expression of KIM-1 in renal tissue by using immunohistochemical techniques and found that administration of RA reduced the elevated expression of KIM-1 in CP-induced AKI.…”

Section: Discussionmentioning

confidence: 94%

“…A single injection of CP at the dose of 20 mg/kg in normal saline was administered intraperitoneally (ip) to mice to generate the CP-induced AKI model 45 , 54 – 56 . RA at the dose of 100 mg/kg dissolved in water was given to mice orally for two consecutive days after 24 h of CP injection.…”

Section: Methodsmentioning

confidence: 99%

“…RA at the dose of 100 mg/kg dissolved in water was given to mice orally for two consecutive days after 24 h of CP injection. CP and RA dose schedules were based on previously published reports 45 , 57 , 58 . Twenty-four animals were randomly divided into four groups ( n = 6) as follows.…”

Section: Methodsmentioning

confidence: 99%

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NLRP3 inflammasome in rosmarinic acid-afforded attenuation of acute kidney injury in mice

Akhter

Khan

Baghel

et al. 2022

Sci Rep

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Cisplatin (CP) is a well-known anticancer drug used to effectively treat various kinds of solid tumors. CP causes acute kidney injury (AKI) and unfortunately, there is no therapeutic approach in hand to prevent AKI. Several signaling pathways are responsible for inducing AKI which leads to inflammation in proximal convoluted tubule cells in the kidney. Furthermore, the nucleotide-binding oligomerization domain (NOD)-like receptor containing pyrin domain 3 (NLRP3) inflammasome is involved in the CP-induced AKI. In this study, we investigated therapeutic effects of rosmarinic acid (RA) against inflammation-induced AKI. RA was orally administered at the dose of 100 mg/kg for two consecutive days after 24 h of a single injection of CP at the dose of 20 mg/kg administered intraperitoneally in Swiss albino male mice. Treatment of RA inhibited the activation of NLRP3 signaling pathway by blocking the activated caspase-1 and downstream signal molecules such as IL-1β and IL18. CP activated HMGB1-TLR4/MyD88 axis was also found to be downregulated with the RA treatment. Activation of nuclear factor-κB and elevated protein expression of cyclooxygenase-2 (COX-2) were also found to be downregulated in RA-treated animals. Alteration of early tubular injury biomarker, kidney injury molecule-1 (KIM-1), was found to be subsided in RA-treated mice. RA has been earlier reported for antioxidant and anti-inflammatory properties. Our findings show that blocking a critical step of inflammasome signaling pathway by RA treatment can be a novel and beneficial approach to prevent the CP-induced AKI.

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Section: Discussionmentioning

confidence: 94%

Section: Methodsmentioning

confidence: 99%

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NLRP3 inflammasome in rosmarinic acid-afforded attenuation of acute kidney injury in mice

Akhter

Khan

Baghel

et al. 2022

Sci Rep

Self Cite

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“…Moreover, the balance between oxidation and antioxidation can be disturbed, thus generating excessive clusters of reactive oxygen species, aggravating mitochondrial dysfunction, brain homeostatic imbalance, and oxidative stress‐related injury, which can cause abnormal structure of hippocampal tissue and induce cognitive dysfunction 21,22 . Nrf2 is a key transcription factor for cellular redox homeostasis and can enter the nucleus to bind to antioxidant response elements (AREs), which initiate the regulation of downstream anti‐inflammatory factors, antioxidant proteins, immune factors, and many other target genes 23,24 . HO‐1 catalyzes the release of biliverdin through heme catabolism in the presence of oxygen and coenzyme II, thereby inhibiting lipid peroxidation 25 .…”

Section: Discussionmentioning

confidence: 99%

The effect of TEMPOL pretreatment on postoperative cognitive function, inflammatory response, and oxidative stress in aged rats under sevoflurane anesthesia

Liu,

Chen,

Gong

et al. 2023

Immunity Inflam & Disease

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IntroductionThe heterocyclic compound 4‐hydroxy‐(2,2,6,6‐Tetramethylpiperidin‐1‐yl)oxyl (TEMPOL) has a protective effect on neurological function in brain tissues damaged by ischemia and hypoxia. This study explored the effects of TEMPOL pretreatment on postoperative cognitive function in aged rats under sevoflurane anesthesia, focusing on inflammatory response and oxidative stress.MethodsSixty male rats were divided into normal control (C), sevoflurane anesthesia (S), TEMPOL pretreatment (T), and sevoflurane anesthesia + TEMPOL pretreatment (ST) groups (15 per group). Groups T and ST rats received continuous intraperitoneal TEMPOL (100 mg/kg) for 3 days, while groups C and S rats were injected with 0.9% saline. After pretreatment, groups S and ST received 3% sevoflurane anesthesia.ResultsRats in group S exhibited a longer swimming distance, longer escape latency, lower frequency of platform crossing, and shorter dwell time in the targeted quadrant than those in groups C and T. Rats in group ST exhibited a shorter swimming distance, shorter escape latency, higher frequency of platform crossing, and longer dwell time in the targeted quadrant than those in group S. The expressions of interleukin‐6, tumor necrosis factor‐α, inducible nitric oxide synthase, and Ym1/2 messenger ribonucleic acid were higher in groups S and ST rats than in groups C and T rats and lower in group ST rats than in group S rat (p < .05). Superoxide dismutase (SOD), total antioxidant capacity (T‐AOC), and glutathione peroxidase (GSH‐Px) were lower, while malondialdehyde (MDA) was higher in groups S and ST rats than in groups C and T rats (p < .05). Group ST showed higher SOD, T‐AOC, and GSH‐Px, and lower MDA than group S (p < .05).ConclusionsTEMPOL pretreatment attenuated postoperative cognitive impairment induced by sevoflurane anesthesia in aged rats. This may be attributed to the downregulation of NR2B‐CREB‐BDNF pathway, reducing the inflammatory response and oxidative stress damage in hippocampal tissue.

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“…Furthermore, water imbalance regulated by AQP2-AVPR2 has been associated with a variety of pathophysiological states, most of which are associated with altered urinary concentrating ability, such as renal ischemia/reperfusion injury [36], cisplatin-induced nephropathy [37], gentamicin-induced nephropathy [38], urinary tract obstruction [39], nephrotic syndrome [40], chronic heart failure [41], and renal disease [42]. CKD was a chronic disease characterized by hypertension, urinary concentrating abnormalities, and electrolyte imbalances which including polyuria, hypercalcemia, hypernatremia, and hypokalemia caused by changes in AQP2 and AVPR2 expression [43][44][45][46].…”

Section: Discussionmentioning

confidence: 99%

Comparative quantitation of aquaporin-2 and arginine vasopressin receptor-2 localizations among chronic kidney disease and healthy kidney in dogs

et al. 2021

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Background and Aim: Aquaporin-2 (AQP2) and arginine vasopressin receptor-2 (AVPR2) are proteins that control water homeostasis in principal cells. Chronic kidney disease (CKD) is defined as the impairment and irreversible loss of kidney function and/or structure, which causes water imbalances and polyuria. The study aimed to know the expression of AQPs and AVPR2 in the kidneys of a canine with CKD. Materials and Methods: The kidneys were collected from two dog carcasses from Small Animal Teaching Hospital, Faculty of Veterinary Medicine, Chiang Mai University. The kidney tissue was prepared for immunohistochemistry and investigated the expression and localization of tissue's AQP2 and AVPR2. For statistical analysis, the Mann–Whitney U-test was applied to the data. Results: By immunohistochemistry, AQP2 was expressed strongly in the basolateral and apical membranes of the principal cells, whereas AVPR2 was localized in the principal cell's basolateral membrane in both renal cortex and renal medulla. In the normal kidney, the semi-quantitative immunohistochemistry for the percentage of protein expression of AQP2 and AVPR2 was 5.062±0.4587 and 4.306±0.7695, respectively. In contrast, protein expression of AQP2 and AVPR2 in CKD was found to be 1.218±0.1719 and 0.8536±0.1396, respectively. The data shows that the percentage of AQP2 and AVPR2 expression was decreased, corresponding to a 4-fold and 5-fold in CKD (p<0.001). Conclusion: Our findings revealed that CKD was a marked decrease in AQP2 and AVPR2 expression. The central role of specific AQP2 and AVPR2 in regulating water homeostasis will provide correlations in case of CKD with polyuria.

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Tempol (4-hydroxy tempo) protects mice from cisplatin-induced acute kidney injury via modulation of expression of aquaporins and kidney injury molecule-1

Cited by 10 publications

References 43 publications

NLRP3 inflammasome in rosmarinic acid-afforded attenuation of acute kidney injury in mice

NLRP3 inflammasome in rosmarinic acid-afforded attenuation of acute kidney injury in mice

The effect of TEMPOL pretreatment on postoperative cognitive function, inflammatory response, and oxidative stress in aged rats under sevoflurane anesthesia

Comparative quantitation of aquaporin-2 and arginine vasopressin receptor-2 localizations among chronic kidney disease and healthy kidney in dogs

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