Thymoquinone and curcumin combination protects cisplatin-induced kidney injury, nephrotoxicity by attenuating NFκB, KIM-1 and ameliorating Nrf2/HO-1 signalling

Fayi, Majed Al; Otifi, Hassan; Alshyarba, Mishari; Dera, Ayed A.; Rajagopalan, Prasanna

doi:10.1080/1061186x.2020.1722136

Cited by 57 publications

(41 citation statements)

References 44 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Cisplatin-induced kidney damage can activate macrophages triggered inflammation resulting in the production of an array of inflammatory related cytokines, including TNF-α, IL-1β and IL-6 (Hagar et al 2015). The results from this study are in accordance and consistent with the previous studies indicating the toxicity of CP in renal tissues by increasing the levels of pro-inflammatory cytokines (Hagar et al 2015;Al Fayi et al 2020). In agreement with previous studies, our results indicated that CP administration caused significant increase in pro-inflammatory cytokines suggesting the initiation of inflammation.…”

Section: Discussionsupporting

confidence: 92%

N⁶-2-hydroxyethyl-adenosine ameliorate cisplatin induced acute kidney injury in mice

Yin

Olatunji

et al. 2020

All Life

View full text Add to dashboard Cite

N 6-2-hydroxyethyl-adenosine (HEA) is one of the main bioactive components found in Cordyceps cicadae and it has been reported to display antioxidant and anti-inflammatory activities. Cisplatin (CP) is one of the most commonly used chemotherapeutic drug for treating various cancers and tumors, but the use is widely curtailed due to its toxicity of various organs including the kidney. This study was aimed at investigating the protective effect of HEA on cisplatin-induced kidney injury. Mice were pretreated with HEA for 7 days and administered with cisplatin. Kidney function index including blood urea nitrogen (BUN), creatinine, renal oxidative stress and pro-inflammatory indices such as malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), tumor necrosis factor (TNF-α), interleukin 1 beta (IL-1β) and interleukin 6 (IL-6) were measured. Histopathological assessment of the kidney was also performed. The results indicated that HEA noticeably modulated the levels of BUN and creatinine as well as decreased the expression of MDA, TNF-α, IL-1β and IL-6 in the kidney. In addition, HEA up regulated the activities of antioxidant enzymes SOD, CAT and GSH-Px. Therefore, we concluded that HEA could effectively alleviate cisplatin-induced nephrotoxicity by counteracting oxidative stress and inflammation.

show abstract

Section: Discussionsupporting

confidence: 92%

N⁶-2-hydroxyethyl-adenosine ameliorate cisplatin induced acute kidney injury in mice

Yin

Olatunji

et al. 2020

All Life

View full text Add to dashboard Cite

show abstract

“…In addition, Tq has been proven for its nephroprotective effects of kidney mitochondria in oxonic acid‐induced hyperuricemia rats (Dera, Rajagopalan, Alfhili, Ahmed, & Chandramoorthy, 2019). The compound has been recently proven for its synergistic beneficial effects along with curcumin in cisplatin‐induced acute kidney injury (Al Fayi, Otifi, Alshyarba, Dera, & Rajagopalan, 2020).…”

Section: Introductionmentioning

confidence: 99%

Thymoquinone attenuates IgE‐mediated allergic response via pi3k‐Akt‐NFκB pathway and upregulation of the Nrf2‐HO1 axis

et al. 2020

Self Cite

View full text Add to dashboard Cite

IgE‐dependent reactions mediate the majority of allergic diseases. This study explores the effects of thymoquinone (Tq) on IgE‐mediated allergic response in activated mast cells, basophils, and neutrophils. Tq treatment resulted in a dose‐dependent decrease in levels of TNF‐α and IL‐4 in activated RBL‐2H3 cells. Tq inhibited the degranulation of these cells with an IC50 value of 56.37 µM. Moreover, the compound suppressed basophil activation induced through FcεRI receptors with an IC50 value of 45.76 µM in heparinized human whole blood. Likewise, neutrophil migration and elastase activity were dose‐dependently reduced. While Tq decreased the phosphorylation of Akt and NFκB in activated RBL‐2H3 cells, it increased nuclear Nrf2 and HO‐1 antioxidant proteins. Our results indicate that Tq possesses demonstrable activity in cellular models of IgE‐mediated allergic reactions. Practical applications The current study sheds light on the mechanistic pathways of Tq on IgE‐based response in activated mast cells, basophils, and neutrophils. The output of this preclinical in vitro study may be translated into better chemotherapeutic applications of Tq and its analogs in the treatment of allergic inflammation. However, a detailed investigation of in vivo models is recommended.

show abstract

“…HO‐1 is a stress‐regulated protein induced by Nrf2 protects against the cytotoxicity of various oxidative stresses response. Nrf2 as a signaling protein can up‐regulate antioxidant enzymes, thereby reducing oxidative stress caused by ROS 11,34,35 . Moreover, previous study displayed that cisplatin damaged anti‐oxidant defense mechanisms followed by an apparent reduce in GSH and increase in MDA levels.…”

Section: Discussionmentioning

confidence: 98%

“…Previous studies demonstrated that overproduction of reactive oxygen species (ROS) may result in lipid peroxidation and delayed renal damage 10 . In addition, nuclear factor erythroid 2‐related factor 2 (Nrf2) is a signaling protein that helps in upregulation of the antioxidant enzymes through heme oxygenase‐1 (HO‐1) protein to counteract the oxidative stress caused by ROS 11 . Until now, growing evidences indicate that indexes of oxidative stress including glutathione (GSH) and malondialdehyde (MDA) also contribute to pathology process of cisplatin‐induced nephrotoxicity.…”

Section: Introductionmentioning

confidence: 99%

Protective effect of ginsenoside Rk1, a major rare saponin from black ginseng, on cisplatin‐induced nephrotoxicity in HEK‐293 cells

Jiang

et al. 2020

The Kaohsiung J of Med Scie

View full text Add to dashboard Cite

Cisplatin, as one of the most effective chemotherapeutic agents, its clinical use is limited by serious side effect of nephrotoxicity. Cisplatin‐induced nephrotoxicity is closely related to apoptosis induction and activation of caspase. The present study aimed to explore the potential protective effect of ginsenoside Rk1 (Rk1), a rare ginsenoside generated during steaming ginseng, on cisplatin‐induced nephrotoxicity and the underlying mechanisms in human embryonic kidney 293 (HEK‐293) cells. Our results showed that the reduced cell viability induced by cisplatin could significantly recover by Rk1. Furthermore, glutathione (GSH) as an oxidative index, was elevated and the lipid peroxidation product malondialdehyde (MDA) was significantly decreased after Rk1 treatment compared to the cisplatin group. Additionally, Rk1 can also decrease the ROS fluorescence expression and increase the protein levels of nuclear factor erythroid 2‐related factor 2 (Nrf2) and heme oxygenase‐1 (HO‐1) compared to the cisplatin group, which suggested a suppression of oxidative response. More importantly, the cisplatin‐induced elevated protein levels of Bax, cleaved caspase‐3, cleaved caspase‐9, and decreased protein level of Bcl‐2 were reversed after treatment with Rk1. Our results elucidated the possible protective mechanism of Rk1 for the first time, which may involve in its anti‐oxidation and anti‐apoptosis effects.

show abstract

Thymoquinone and curcumin combination protects cisplatin-induced kidney injury, nephrotoxicity by attenuating NFκB, KIM-1 and ameliorating Nrf2/HO-1 signalling

Abstract: Supplementary figure 1: Hematoxylin and Eosin staining of rat kidney sections with. (a) 50 mg/kg bw Thymoquinone (Tq), (b) 100 mg/kg bw curcumin (Cur) showing no signs of toxicity in the kidney tissues.

Cited by 57 publications

References 44 publications

N⁶-2-hydroxyethyl-adenosine ameliorate cisplatin induced acute kidney injury in mice

N⁶-2-hydroxyethyl-adenosine ameliorate cisplatin induced acute kidney injury in mice

Thymoquinone attenuates IgE‐mediated allergic response via pi3k‐Akt‐NFκB pathway and upregulation of the Nrf2‐HO1 axis

Protective effect of ginsenoside Rk1, a major rare saponin from black ginseng, on cisplatin‐induced nephrotoxicity in HEK‐293 cells

Contact Info

Product

Resources

About

Thymoquinone and curcumin combination protects cisplatin-induced kidney injury, nephrotoxicity by attenuating NFκB, KIM-1 and ameliorating Nrf2/HO-1 signalling

Abstract: Supplementary figure 1: Hematoxylin and Eosin staining of rat kidney sections with. (a) 50 mg/kg bw Thymoquinone (Tq), (b) 100 mg/kg bw curcumin (Cur) showing no signs of toxicity in the kidney tissues.

Cited by 57 publications

References 44 publications

N6-2-hydroxyethyl-adenosine ameliorate cisplatin induced acute kidney injury in mice

N6-2-hydroxyethyl-adenosine ameliorate cisplatin induced acute kidney injury in mice

Thymoquinone attenuates IgE‐mediated allergic response via pi3k‐Akt‐NFκB pathway and upregulation of the Nrf2‐HO1 axis

Protective effect of ginsenoside Rk1, a major rare saponin from black ginseng, on cisplatin‐induced nephrotoxicity in HEK‐293 cells

Contact Info

Product

Resources

About

N⁶-2-hydroxyethyl-adenosine ameliorate cisplatin induced acute kidney injury in mice

N⁶-2-hydroxyethyl-adenosine ameliorate cisplatin induced acute kidney injury in mice