Vetiver oil (Java) attenuates cisplatin-induced oxidative stress, nephrotoxicity and myelosuppression in Swiss albino mice

Sinha, Shivam; Jothiramajayam, Manivannan; Ghosh, Manosij; Jana, Aditi; Chatterji, Urmi; Mukherjee, Anita

doi:10.1016/j.fct.2015.04.018

Cited by 33 publications

(20 citation statements)

References 39 publications

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“…It has been reported that cisplatin-induced oxidative stress plays an important role in producing myelosuppression. [51][52][53][54][55] Therefore, reducing the severity of cisplatin-induced oxidative stress might have an effect on inhibiting myelosuppression. We found that avonoids and alkaloids in HWKL can reduce cisplatin-induced oxidative stress and apart from these, ginsenosides in GR (such as 19, 20, 26 in Fig.…”

Section: Discussionmentioning

confidence: 99%

He-Wei granules (HWKL) combat cisplatin-induced nephrotoxicity and myelosuppression in rats by inhibiting oxidative stress, inflammatory cytokines and apoptosis

et al. 2017

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Section: Discussionmentioning

confidence: 99%

He-Wei granules (HWKL) combat cisplatin-induced nephrotoxicity and myelosuppression in rats by inhibiting oxidative stress, inflammatory cytokines and apoptosis

et al. 2017

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“…However, despite their effectiveness, some antineoplasic drugs have limited use because of their adverse side effects, including neurotoxicity, nephrotoxicity, myelosuppresion, etc. (Li et al 2015;Sinha et al 2015). Therefore, treatment improvement with use of alternative compounds to reduce these undesirable effects has become imperative.…”

Section: Introductionmentioning

confidence: 99%

Cytotoxic and toxicogenomic effects of silibinin in bladder cancer cells with different TP53 status

et al. 2016

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Silibinin is a natural phenol found in the seeds of the milk thistle plant. Recent data have shown its effectiveness for preventing/treating bladder tumours. Therefore, in this study we investigated the cytotoxic and toxicogenetic activity of silibinin in bladder cancer cells with different TP53 statuses. Two bladder urothelial carcinoma cell lines were used: RT4 (wild-type TP53 gene) and T24 (mutated TP53 gene). Cell proliferation, clonogenic survival, apoptosis rates, genotoxicity and relative expression profile of FRAP/mTOR, FGFR3, AKT2 and DNMT1 genes and of miR100 and miR203 were evaluated. Silibinin promoted decreased proliferation and increased late apoptosis in TP53 mutated cells. Increased early apoptosis rates, primary DNA damage, and decrease of cell colonies in the clonogenic survival assay were detected in both RT4 and T24 cell lines. Down-regulation of FRAP/mTOR, AKT2, FGFR3, DNMT1 and miR100 expression occurred in RT4 cells. Modulation of miR203 was observed in both cell lines. In conclusion, despite the reduction of clone formation in both cell lines, the toxicogenomic effect of silibinin on FRAP/mTOR, AKT2, FGFR3, DNMT1 and miR100 was dependent on the TP53 status. Taken together, the data confirmed the role of silibinin as an antiproliferative compound, whose mechanism of action was related to the TP53 status.

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“…Oxidative stress is thought to play a key role in the pathogenesis of nephrotoxicity both in vivo and in vitro (Casanova et al, ; Sinha et al, ). When there is an imbalance between ROS production and antioxidant defense system, oxidative stress occurs, and the antioxidant capacity of the cells is overwhelmed.…”

Section: Discussionmentioning

confidence: 99%

Rutin attenuates vancomycin‐induced renal tubular cell apoptosis via suppression of apoptosis, mitochondrial dysfunction, and oxidative stress

Dai

Guo

et al. 2019

Phytotherapy Research

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Vancomycin is a glycopeptide antibiotic widely used to treat infections caused by methicillin-resistant Staphylococcus aureus. However, nephrotoxicity is a major adverse side effect, and the development of effective nephroprotective agents remains a priority in antimicrobial chemotherapy. In this study, we investigated the cell protective effects of the flavonol glycoside rutin against vancomycin-induced toxicity. Vancomycin added to porcine renal tubular LLC-PK1 cells caused an increase of production of intracellular reactive oxygen species and subsequent apoptotic cell death. Pretreatment of LLC-PK1 cells with rutin at 5, 10, and 20 μM for 2 hr prior to 2-mM vancomycin exposure for 24 hr significantly decreased intracellular reactive oxygen species and increased superoxide dismutase and catalase activities. Rutin pretreatment also protected cells from vancomycin-induced caspase activation, mitochondrial membrane depolarization, and subsequent apoptosis. This study demonstrates a protective effect of rutin and suggests that rutin coadministration is an alternative therapy for treatment of vancomycin-induced nephrotoxicity.

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Vetiver oil (Java) attenuates cisplatin-induced oxidative stress, nephrotoxicity and myelosuppression in Swiss albino mice

Cited by 33 publications

References 39 publications

He-Wei granules (HWKL) combat cisplatin-induced nephrotoxicity and myelosuppression in rats by inhibiting oxidative stress, inflammatory cytokines and apoptosis

He-Wei granules (HWKL) combat cisplatin-induced nephrotoxicity and myelosuppression in rats by inhibiting oxidative stress, inflammatory cytokines and apoptosis

Cytotoxic and toxicogenomic effects of silibinin in bladder cancer cells with different TP53 status

Rutin attenuates vancomycin‐induced renal tubular cell apoptosis via suppression of apoptosis, mitochondrial dysfunction, and oxidative stress

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