The protective role of tetramethylpyrazine against cisplatin-induced ototoxicity

Bayram, Ali̇; Kaya, Altan; Akay, Ebru; Hıra, İbrahim; Özcan, İbrahim

doi:10.1016/j.ijporl.2017.01.005

Cited by 6 publications

(7 citation statements)

References 20 publications

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“…Despite the ototoxic side effect, cisplatin is still the cornerstone treatment for several types of cancer because of the extraordinary anti-tumor effect. Hence, prevention of ototoxicity has been an important goal, and several studies have tried to find ways to minimize the ototoxic effects of cisplatin [22,52,[69][70][71][72]. Since Reactive Oxygen Species (ROS) is thought to play an important role in cisplatin-related ototoxicity, free radical scavengers are suggested as possible otoprotectants.…”

Section: Prevention Of Ototoxicitymentioning

confidence: 99%

Long-term ototoxicity in women after cisplatin treatment for ovarian germ cell cancer

Skalleberg

Solheim

Fosså

et al. 2017

Gynecologic Oncology

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Section: Prevention Of Ototoxicitymentioning

confidence: 99%

Long-term ototoxicity in women after cisplatin treatment for ovarian germ cell cancer

Skalleberg

Solheim

Fosså

et al. 2017

Gynecologic Oncology

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“…It has been shown to possess numerous biological features such as anticoagulation, inhibition of platelet aggregation, anti-inflammation, capillary dilatation, improvement in microcirculation, and protection against reactive oxygen radicals [Zhao et al, 2016]. TMP was also reported to have potential protective effects against ototoxicity [Cui et al, 2015;Bayram et al, 2017]. In the present study, we aimed to investigate the protective effect of TMP against radiation-induced ototoxicity.…”

Section: Introductionmentioning

confidence: 97%

Tetramethylpyrazine Attenuates Radiation-Induced Ototoxicity in a Rat Model

et al. 2023

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Introduction: Tetramethylpyrazine (TMP) is a chemical compound, which has been shown to possess numerous biological features such as anticoagulation, inhibition of platelet aggregation, anti-inflammation, capillary dilatation, improvement in microcirculation, and protection against reactive oxygen radicals. The aim of the present study was to investigate the protective effect of TMP against radiation-induced ototoxicity. Materials and Methods: 40 rats were divided into four groups. The first group was irradiated for 5 days. The second group received a single dose of 140 mg/kg/day intraperitoneal TMP given to the rats 30 min before radiotherapy (RT) for 5 days. The third group received a single dose of 140 mg/kg/day i.p. TMP for 5 days, whereas the fourth group was administered saline. All rats underwent distortion product otoacoustic emission (DPOAE) and auditory brainstem response measurements before and after the application. The temporal bulla of animals was removed for immunohistopathological examination. Results: Signal-noise ratio values were significantly decreased in the RT group for the frequencies of 2–32 kHz after RT (p < 0.05), whereas the difference was not significant in terms of pre- and posttreatment values for the other groups. Also in the RT group, the ABR thresholds were significantly increased after treatment. In H&E staining, the mean scores for outer hair cells (OHCs), stria vascularis (SV), and spiral ganglion (SG) injuries were significantly higher in RT and RT + TMP groups than in the other groups. The mean OHCs and SV injury scores were also significantly higher in the RT group than in the RT + TMP group (p < 0.05). The number of cochleas that showed cytoplasmic caspase-3 immunoreactivity in the OHC, SV, and SG was significantly higher in RT and RT + TMP groups than in the other groups. Conclusion: The findings of the present study suggest that TMP may have a therapeutic potential for preventing sensorineural hearing loss (SNHL) related to RT.

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“…Several drugs with antagonistic effects against cisplatininduced cytotoxicity, dna damage, and apoptosis in cochlear hair cells might represent potential treatment strategies for cisplatin-induced ototoxicity (10,(12)(13)(14). For instance, tetramethylpyrazine (Tet) and tanshinone iia (Tan iia) can protect against hearing impairment and ototoxicity induced by aminoglycoside antibiotics, cisplatin, and radiation (15)(16)(17). Tet can also decrease caspase-3 expression in spiral ganglion and apoptosis in guinea pig cochlea (15,17).…”

Section: Introductionmentioning

confidence: 99%

“…For instance, tetramethylpyrazine (Tet) and tanshinone iia (Tan iia) can protect against hearing impairment and ototoxicity induced by aminoglycoside antibiotics, cisplatin, and radiation (15)(16)(17). Tet can also decrease caspase-3 expression in spiral ganglion and apoptosis in guinea pig cochlea (15,17). Tan iia has been reported to protect House ear institute-organ of corti 1 (Hei-oc1) auditory cells from cisplatin-induced ototoxicity and may synergize with cisplatin, enhancing cytotoxicity against cancer cells by promoting apoptosis and cell cycle arrest at the S phase (18).…”

Section: Introductionmentioning

confidence: 99%

Identifying the mechanisms underlying the protective effect of tetramethylpyrazine against cisplatin‑induced in vitro ototoxicity in HEI‑OC1 auditory cells using gene expression profiling

et al. 2020

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Sensorineural hearing loss is prevalent in patients receiving cisplatin therapy. Tetramethylpyrazine (Tet) and tanshinone iia (Tan iia) have protective roles against hearing impairment or ototoxicity. The present study aimed to investigate the molecular mechanisms underlying cisplatin-induced ototoxicity and the protective effect of Tet and Tan iia against it. House ear institute-organ of corti 1 auditory cells were treated with titrating doses of Tan iia, Tet, and cisplatin. in a cell viability assay, cisplatin, Tan iia and Tet had ic 50 values of 42.89 µM, 151.80 and 1.04x10 3 mg/l, respectively. Tan iia augmented cisplatin-induced cytotoxicity. However, Tet concentrations <75 mg/l attenuated cisplatin-induced cytotoxicity and apoptosis. Moreover, rna sequencing analysis was carried out on auditory cells treated for 30 h with 30 µM cisplatin alone for 48 h or combined with 37.5 mg/l Tet for 30 h. differentially expressed genes (deGs) induced in these conditions were identified and examined using Gene Ontology and Kyoto encyclopedia of Genes and Genomes pathway analysis. cisplatin increased the expression of genes related to the p53 and Foxo pathways, such as Fas, p21/cdKn1a, and Bcl-2 binding component 3, but decreased the expression of insulin-like growth factor 1 (iGF1), as well as genes in the histone (Hist)1 and Hist2 clusters. Treatment with Tet downregulated FoXo3 and Bcl-2 binding component 3, and increased the expression of iGF1. Moreover, Tet upregulated genes associated with Wnt signaling, but not p53-related genes. Thus, the otoprotective properties of Tet might be mediated by activation of Wnt and iGF1 signaling, and inhibition of Foxo signaling.

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The protective role of tetramethylpyrazine against cisplatin-induced ototoxicity

Cited by 6 publications

References 20 publications

Long-term ototoxicity in women after cisplatin treatment for ovarian germ cell cancer

Long-term ototoxicity in women after cisplatin treatment for ovarian germ cell cancer

Tetramethylpyrazine Attenuates Radiation-Induced Ototoxicity in a Rat Model

Identifying the mechanisms underlying the protective effect of tetramethylpyrazine against cisplatin‑induced in vitro ototoxicity in HEI‑OC1 auditory cells using gene expression profiling

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