Omeprazole protects against cisplatin-induced nephrotoxicity by alleviating oxidative stress, inflammation, and transporter-mediated cisplatin accumulation in rats and HK-2 cells

Gao, Huan; Zhang, Sixi; Hu, Tingting; Qu, Xiaoyu; Zhai, Jinghui; Zhang, Yueming; Tao, Lina; Yin, Jianyuan; Song, Yanqing

doi:10.1016/j.cbi.2018.11.008

Cited by 35 publications

(30 citation statements)

References 32 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Moreover, cisplatin treatment led to a significant increase in renal MDA concentration and a decrease in TAC, which indicates cisplatin-induced oxidative stress in renal tissue. These results were consistent with previous studies that reported similar outcomes of cisplatin toxicity [ 17 , 18 , 19 ]. Quinacrine efficiently reversed cisplatin-induced nephrotoxicity phenotype.…”

Section: Discussionsupporting

confidence: 93%

Quinacrine Ameliorates Cisplatin-Induced Renal Toxicity via Modulation of Sirtuin-1 Pathway

El-Magd

Ebrahim

El-Sherbiny

et al. 2021

IJMS

View full text Add to dashboard Cite

Renal toxicity is a serious side effect that hinders the use of cisplatin, a commonly used and effective chemotherapeutic agent. Meanwhile, quinacrine is an FDA approved drug that has been stated for its anti-inflammatory effect. Thus, we investigated the ameliorative effect of quinacrine against cisplatin-induced renal toxicity. Single intraperitoneal (i.p.) 10 mg/kg cisplatin administration induced renal injury in rats. Our results showed that 10 mg/kg/day quinacrine decreased the mortality rate of rats from 46.15% (cisplatin group) to 12.5%, and significantly decreased renal tissue fibrosis, relative kidney to body weight ratio, serum creatinine and urea levels compared with the cisplatin group. Indeed, quinacrine significantly decreased renal malondialdehyde concentration and increased renal total antioxidant capacity, compared with the cisplatin group. Furthermore, quinacrine caused significant upregulation of renal sirtuin-1 (SIRT-1) with significant downregulation of intercellular adhesion molecule-1 (ICAM-1) and tumor necrosis factor-α (TNF-α). Moreover, quinacrine significantly blocked cisplatin-induced apoptosis, which was made evident by downregulating renal apoptotic proteins (BAX and p53) and upregulating the renal anti-apoptotic protein BCL2, compared with the cisplatin group. In conclusion, this study demonstrates, for the first time, that quinacrine alleviates cisplatin-induced renal toxicity via upregulating SIRT-1, downregulating inflammatory markers (ICAM-1 and TNF-α), reducing oxidative stress, and inhibiting apoptosis.

show abstract

Section: Discussionsupporting

confidence: 93%

Quinacrine Ameliorates Cisplatin-Induced Renal Toxicity via Modulation of Sirtuin-1 Pathway

El-Magd

Ebrahim

El-Sherbiny

et al. 2021

IJMS

View full text Add to dashboard Cite

show abstract

“…Previous studies showed that the expression of inflammatory cytokines is elevated in the kidney after cisplatin injury (Miller et al, 2010). The levels of several pro-inflammatory cytokines, such as TNF-α and IL-1β, were found to be elevated in the urine of cisplatin-treated mice (Gao et al, 2019;Güntürk Quantitative image analysis for immunohistochemical staining expressed as area percent across 10 different fields for each rat section. Values are given as mean ± SD of six observations, a or b: Statistically significant from the control or the cisplatin group, respectively at p < 0.05 using ANOVA followed by Tukey-Kramer as a post-hoc test.…”

Section: Discussionmentioning

confidence: 99%

“…These include the inhibition of macrophage and T cell infiltration, M1/M2 transition and cytokine expression (Jiandong et al, 2009;Piggott et al, 2011;Hans et al, 2012). Indeed, the treatment with anti-inflammatory agents is a promising strategy in reducing cisplatin-induced renal dysfunction and decreasing the histological evidence of injury (El-Naga, 2014;El-Naga and Mahran, 2016;Gao et al, 2019;Güntürk et al, 2019;Iwakura et al, 2019;Michel and Menze, 2019;Soetikno et al, 2019).…”

Section: Discussionmentioning

confidence: 99%

“…Remarkably, the oxidative stress is actively involved in the pathogenesis of cisplatin-induced acute renal injury and immensely drives to apoptotic cell death both in vitro (Yang et al, 2019) and in vivo (Badawy et al, 2019;Soetikno et al, 2019). Also, there are multiple suggestion about the involvement of pro-inflammatory cytokines in the pathogenesis of cisplatin-induced nephrotoxicity (Gao et al, 2019;Güntürk et al, 2019;Iwakura et al, 2019;Michel and Menze, 2019;Soetikno et al, 2019). Indeed, searching for other pathways that may be engaged in the pathogenesis of cisplatin renal injury is required for finding new promising protective strategies against this deleterious effect.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Dibenzazepine Attenuates Against Cisplatin-Induced Nephrotoxicity in Rats: Involvement of NOTCH Pathway

et al. 2020

View full text Add to dashboard Cite

Cisplatin is one of the standard anti-cancer agents that are used to treat variety of solid tumors. Nevertheless, due to the accumulation of cisplatin in the renal epithelial cells, nephrotoxicity was found to be the main side effect that limits its clinical use. The current study was conducted to assess the potential nephroprotective effect of dibenzazepine, a Notch inhibitor, against cisplatin-induced nephrotoxicity in rats as well as the possible mechanisms underlying this nephroprotection. The rats were pre-treated with 2 mg/kg dibenzazepine for 7 days before giving a single nephrotoxic dose of cisplatin (7 mg/kg). Cisplatin induced acute nephrotoxicity, where blood urea nitrogen and serum creatinine levels were significantly increased. Besides, lipid peroxidation was markedly elevated and the levels of reduced glutathione and catalase were significantly reduced. Also, the tissue levels of the pro-inflammatory mediators; IL-1β, TNF-α, and NF-kB, were significantly increased in the cisplatin group. The pre-treatment with dibenzazepine significantly mitigated the nephrotoxic effects of cisplatin, the oxidative stress and inflammatory status as well as decreased caspase-3 expression, as compared to the cisplatin group. Furthermore, the up-regulation of Notch-1 and Hes-1 was found to be involved in cisplatin-induced nephrotoxicity and their expression was significantly reduced by dibenzazepine. The nephroprotective effect of dibenzazepine was further confirmed by the histopathological assessment. Moreover, dibenzazepine pre-treatment of hela and PC3 cells in vitro did not antagonize the cisplatin anti-cancer activity. In conclusion, these findings show that dibenzazepine provides protection against cisplatin-induced nephrotoxicity. Moreover, the up-regulation of the Notch pathway was shown to play a role in the pathogenesis of cisplatin-induced renal injury.

show abstract

“…Solid carrier membrane proteins are expressed to maintain metabolism balance of the cell by mediating the transport of exogenous and endogenous substances. Decreased expression levels of, hMATE1 (SLC47A1), hOCT3 (SLC22A3), and hMATE2-K (SLC47A2) are responsible from oxaliplatin transport, resulting in oxaliplatin resistance (34). Apart from the above, transforming growth factor β1 (TGF-β1) is secreted by cells within in tumor microenvironment.…”

Section: Drug Resistance In Colorectal Cancermentioning

confidence: 99%

Drug Resistance Mechanisms on Colorectal Cancer

Kurter

Yeşil²,

Daskin

et al. 2021

Journal of Basic and Clinical Health Sciences

View full text Add to dashboard Cite

Standard treatment for colorectal cancer includes surgery, radiotherapy, and chemotherapy. Conventional chemotherapeutic agents used in colorectal cancer such as 5-fluorouracil, capecitabine which is oral form of 5-fluorouracil, irinotecan, and oxaliplatin. One of the major challenges in chemotherapy considered as drug resistance. Drug resistance occurs in many different mechanisms such as alteration in tumor microenvironment, growth kinetics, genetic variations, and tumor heterogeneity. These cytotoxic agents are used in combination form to overcome drug resistance on colorectal cancer. They can also be used in combination with cytotoxic agents as bevacizumab and cetuximab. Combination therapy depends on tumor burden, type, stage, and molecular characteristics. It is crucial to choose the combination therapy to be applied by taking these factors into consideration. In this review, current drug resistance mechanisms were discussed and then mechanisms of conventional chemotherapy related resistance were explained.

show abstract

Omeprazole protects against cisplatin-induced nephrotoxicity by alleviating oxidative stress, inflammation, and transporter-mediated cisplatin accumulation in rats and HK-2 cells

Cited by 35 publications

References 32 publications

Quinacrine Ameliorates Cisplatin-Induced Renal Toxicity via Modulation of Sirtuin-1 Pathway

Quinacrine Ameliorates Cisplatin-Induced Renal Toxicity via Modulation of Sirtuin-1 Pathway

Dibenzazepine Attenuates Against Cisplatin-Induced Nephrotoxicity in Rats: Involvement of NOTCH Pathway

Drug Resistance Mechanisms on Colorectal Cancer

Contact Info

Product

Resources

About

Omeprazole protects against cisplatin-induced nephrotoxicity by alleviating oxidative stress, inflammation, and transporter-mediated cisplatin accumulation in rats and HK-2 cells

Cited by 35 publications

References 32 publications

Quinacrine Ameliorates Cisplatin-Induced Renal Toxicity via Modulation of Sirtuin-1 Pathway

Quinacrine Ameliorates Cisplatin-Induced Renal Toxicity via Modulation of Sirtuin-1 Pathway

Dibenzazepine Attenuates Against Cisplatin-Induced Nephrotoxicity in Rats: Involvement of NOTCH Pathway

Drug Resistance Mechanisms on Colorectal Cancer

Contact Info

Product

Resources

About

Omeprazole protects against cisplatin-induced nephrotoxicity by alleviating oxidative stress, inflammation, and transporter-mediated cisplatin accumulation in rats and HK-2 cells