Ccrn4l as a pre-dose marker for prediction of cisplatin-induced hepatotoxicity susceptibility

Hwang, Da Bin; Won, Dong Hoon; Shin, Yoo Sub; Kim, Shin Young; Kang, Byeong Cheol; Lim, Kyung Min; Hwan, Jeong; Nam, Ki Taek; Yun, Jun Won

doi:10.1016/j.freeradbiomed.2020.01.003

Cited by 12 publications

(12 citation statements)

References 40 publications

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“…Although cisplatin (CP) [ cis -diamminedichloroplatinum (II), CDDP], is potent anticancer medication use to treat a variety of tumors including testicular, ovarian, bladder, and lung ( Ibrahim et al., 2016 ; Karwasra et al., 2016 ). Several recent studies recorded that the CP induces hepatotoxicity ( Abdellatief et al., 2017 ; Qu et al., 2019 ; Abdel-Daim et al., 2020 ; Hwang et al., 2020 ) and nephrotoxicity ( Abdel-Daim et al., 2017 ; Abdel-Razek et al., 2020 ; Abo-Elmaaty et al., 2020 ; Sadeghi et al., 2020 ). Miller et al.…”

Section: Introductionmentioning

confidence: 99%

L-Carnitine Mitigates Oxidative Stress and Disorganization of Cytoskeleton Intermediate Filaments in Cisplatin-Induced Hepato-Renal Toxicity in Rats

et al. 2020

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Cisplatin (CP) is one of the most active medications in cancer treatment and has some adverse effects such as hepatotoxicity and nephrotoxicity. The present research was planned to determine the protective effects of L-carnitine (LC) against CP-induced hepatorenal oxidative stress in rats, via investigating of some serum biochemical and tissue oxidative/antioxidant parameters, histological alterations, and immunohistochemical expressions of two different intermediate filaments (IFs) proteins; vimentin (VIM) and cytokeratin 18 (CK18). Twenty-eight rats were divided into four groups (7 rats each). Groups I and II were orally administered saline and LC (100 mg/kg body weight), respectively, once daily for 30 consecutive days. Group III received saline orally once daily and a single dose of CP on the 27th day of the experiment [7.5 mg/kg, intraperitoneal (IP)]. Group IV received both LC and CP. Injection of CP significantly (P ≤ 0.05) increased serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP) activities and creatinine and urea levels, while serum total protein, albumin, and globulin concentrations significantly (P ≤ 0.05) decreased. In addition, CP induced a dramatic increase in the Malondialdehyde (MDA) level along with a substantial decrease in reduced glutathione (GSH) and catalase (CAT) in the hepato-renal tissues. Histologically, both liver and kidney of the CP treated group revealed marked degenerative changes. Moreover, overexpression of both VIM and CK18 in hepato-renal tissues were noted after CP injection. On the other hand, the administration of LC in the CP injected group (Group IV) restored the biochemical parameters, histological, and immunohistochemical pictures toward the normalcy. In conclusion, LC may be supplemented for chemotherapy with CP to ameliorate its oxidative stress and restore

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Section: Introductionmentioning

confidence: 99%

L-Carnitine Mitigates Oxidative Stress and Disorganization of Cytoskeleton Intermediate Filaments in Cisplatin-Induced Hepato-Renal Toxicity in Rats

et al. 2020

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“…The mice were gently grasped, and 5 µL of each solution was treated to the right inferior conjunctival sac, and the eyes were kept open for 60 s. At 12 h after the last treatment, mice were anesthetized with isoflurane and sacrificed, and the eyes were fixed in Davidson's solution for histopathological analysis. In the second experiment using rats, cisplatin was treated to induce hepatotoxicity and nephrotoxicity according to the method of Hwang et al [26] and Hwang et al [27]. Briefly, the experimental group was divided into two groups: normal saline and cisplatin treatment (n = 5 per group).…”

Section: Animal Experimentsmentioning

confidence: 99%

“…According to the methods of Ye et al [28], we treated human corneal epithelial cells with SLS and benzalkonium chloride (BAC) as well as 17 test substances from various chemical classes (6 no category, 3 Cat2B, 2 Cat2A, and 6 Cat1) according to the UN GHS category of irritants [29] (Table 1). After irritant treatments for 10 min and washing with PBS, post-incubation was performed for 6, 12, or 18 h. Cisplatin was treated for 24 h according to the method of Hwang et al [26]. Subsequently, RNA or protein was extracted for further experiments.…”

Section: Cell Culture and Treatmentsmentioning

confidence: 99%

Egr1 Gene Expression as a Potential Biomarker for In Vitro Prediction of Ocular Toxicity

et al. 2021

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Animal models are used for preclinical toxicity studies, and the need for in vitro alternative methods has been strongly raised. Our study aims to elucidate the potential mechanism of change in EGR1 expression under situations of toxic injury and to develop an Egr1 promoter–luciferase gene reporter assay for an in vitro alternative method for toxicity prediction in drug discovery. We first found an increase in early growth response-1 (EGR1) mRNA/protein expressions in the liver and kidney of cisplatin-treated injured rats. Additionally, the EGR1 protein level was also elevated under situations of ocular injury after sodium lauryl sulfate (SLS) eye drops. These in vivo observations on injury-related EGR1 induction were confirmed by in vitro studies, where human corneal epithelial cells were treated with representative irritants (SLS and benzalkonium chloride) and 17 chemicals having different UN GHS irritant categories. Additionally, our results suggest the involvement of ERK, JNK, p38 MAPK pathways in EGR1 elevation in response to gamma-butyrolactone-induced injury. As EGR1 is considered to be a pivotal factor in proliferation and regeneration, siRNA-mediated knockdown of Egr1 promoted cytotoxic potential through a delay of injury-related recovery. More importantly, the elevation of promoter activities was observed by various irritants in cells transfected with Egr1 promoter-reporter vector. In conclusion, Egr1 can be a potential biomarker in a promoter-reporter system to improve the accuracy of in vitro predictions for ocular irritation.

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“…14 Cisplatin [CIS] is a platinum-based chemotherapeutic drug that induces cytotoxicity through the kallikrein-kinin system and leads to inflammatory and oxidative stress 15 . However, CIS has serious side effects such as hepatotoxicity 16 , nephrotoxicity 17 , ototoxicity 18 and neurotoxicity 18 . Therefore, studies to improve chemotherapy efficacy while reducing their side effects are rigorous to be able better to control the metastasis and progressivity of ovarian cancer.…”

Section: Introductionmentioning

confidence: 99%

Curcumin Prevents Epithelial-to Mesenchymal Transition-Mediated Ovarian Cancer Progression through NRF2/ETBR/ET-1 Axis and Preserves Mitochondria Biogenesis in Kidney after Cisplatin Administration

et al. 2020

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Purpose: Ovarian carcinoma is one of the gynaecological malignancies that have the highest mortality rates due to its progressivity. Endothelin signalling plays a leading role in the progression of ovarian cancer through Epithelial-to-Mesenchymal Transition (EMT). Cisplatin commonly used as potent chemotherapy; however, its application hindered by its nephrotoxic effect. Curcumin, a turmeric-derived compound, has an anticancer property, as well as a renal protective effect. Moreover, curcumin augments the affinity of the antioxidant enzyme, while inhibits endothelin-1 (ET-1) signalling. The effects of curcumin on ovarian cancer progression and cisplatin-induced kidney injury remain unknown. Methods: Curcumin was used as a supplementary therapy together with cisplatin in Human Ovarian Cancer Cell line (SKOV3) and also in rodent-induced ovarian cancer. The kidney phenotype in the ovarian cancer rat model after cisplatin ± curcumin administration will also be analyzed Results: Co-treatment of cisplatin with curcumin enhanced the expression of a gene involved in apoptosis in association with NRF2 enhancement, thus activated ETBR-mediated ET-1 clearance in SKOV3 cell and ovarian cancer model in rat. Moreover, curcumin treatment improved mitochondria biogenesis markers such as PGC-1α and TFAM and prevented the elevated of ET-1-mediated renal fibrosis and apoptosis in kidney isolated from cisplatin-treated ovarian cancer rat. Conclusion: Curcumin could be potentially added as an anticancer adjuvant with protective effects in the kidney; thus, improves the efficacy and safety of cisplatin treatment in the clinical setting.

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Ccrn4l as a pre-dose marker for prediction of cisplatin-induced hepatotoxicity susceptibility

Cited by 12 publications

References 40 publications

L-Carnitine Mitigates Oxidative Stress and Disorganization of Cytoskeleton Intermediate Filaments in Cisplatin-Induced Hepato-Renal Toxicity in Rats

L-Carnitine Mitigates Oxidative Stress and Disorganization of Cytoskeleton Intermediate Filaments in Cisplatin-Induced Hepato-Renal Toxicity in Rats

Egr1 Gene Expression as a Potential Biomarker for In Vitro Prediction of Ocular Toxicity

Curcumin Prevents Epithelial-to Mesenchymal Transition-Mediated Ovarian Cancer Progression through NRF2/ETBR/ET-1 Axis and Preserves Mitochondria Biogenesis in Kidney after Cisplatin Administration

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