香芹酮抗紫杉醇所致耳毒性损伤的保护机制研究

IF 0.3 Q4 MEDICINE, RESEARCH & EXPERIMENTAL Clinical and Experimental Health Sciences Pub Date : 2023-09-14 DOI:10.33808/clinexphealthsci.1130449
Büşra DİNCER, Fatma ATALAY, Arzu TATAR
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引用次数: 0

摘要

目的:耳毒性是在癌症等危重疾病中使用固体疗法作为化疗药物引起的细胞损伤。自由基的产生与化疗引起的波动性听力损失有关。抗氧化剂可以帮助防止耳毒性相关的氧化损伤。香芹酮(CVN)是一种具有优异抗氧化性能的单萜,可以防止氧化损伤。本研究探讨了CVN对紫杉醇(PCX)诱导的耳毒性的耳保护机制的生化和功能方面。方法:将24只Wistar白化大鼠分为对照组、CVN组、PCX组、PCX+CVN组。对照组给予生理盐水治疗,每周一次。PCX组腹腔注射PCX 5 mg/kg,每周1次(共4次)。CVN组给予50 mg/kg腹腔注射,每周1次。PCX+ CVN组给予PCX 5 mg/kg后再加CVN 5 mg/kg,每周1次。所有动物在给药前(第0天)和给药后(第23天)分别进行变质产物耳声发射测试。 结果:PCX通过削弱耳声发射值表现出耳毒性作用。PCX导致显著的耳声发射值偏移,CVN共处理(2000Hz p<.001, 4000级p<0.01,适用于6000Hz p<.001,对于8000hz p<PCX+CVN组为0.01)。此外,与其他组相比,PCX组耳蜗组织中丙二醛水平显著升高,谷胱甘肽水平显著降低。CVN与PCX联合使用逆转了这些影响,使氧化应激参数接近对照组(GSH水平p<.001,为MDA水平p<PCX+CVN组为0.01)。 结论:CVN具有保护大鼠耳蜗功能,抵抗PCX的破坏作用。
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Otoprotective Mechanisms of Carvone As An Antioxidant Agent Against Ototoxic Damage Caused By Paclitaxel
Objective: Ototoxicity is cellular damage caused by the use of solid treatments as chemotherapeutics in critical illnesses like cancer. The generation of free radicals is linked to fluctuating hearing loss caused by chemotherapeutics. Antioxidants can help to prevent ototoxicity-related oxidative damage. Carvone (CVN) is a monoterpene with excellent antioxidant properties that protect against oxidative damage. This study investigates the biochemical and functional aspects of CVN’s putative otoprotective mechanisms against paclitaxel (PCX)-induced ototoxicity. Methods: 24 Wistar albino rats were assigned into four different groups: Control, CVN, PCX, and PCX+CVN. Once a week, the control group received saline. The PCX group received 5 mg/kg PCX intraperitoneally once a week (4 times). Once a week, the CVN group received 50 mg/kg intraperitoneally. The PCX+ CVN group received 5 mg/kg PCX followed by 5 mg/kg CVN once a week. All animals were subjected to deterioration product otoacoustic emission testing before (day 0) and after drug administration (day 23). Results: PCX showed an ototoxic effect by weakening otoacoustic emission values. PCX leads to significant otoacoustic emission value shifts ameliorated by CVN co-treatment (for 2000Hz p< .001, for 4000 levels p< .01, for 6000Hz p< .001, and for 8000 Hz p< .01 in PCX+CVN group). Furthermore, the PCX group had significantly greater malondialdehyde levels and significantly lower glutathione levels in the cochlear tissues, compared to the other groups. Co-administered CVN with PCX reversed these effects, making oxidative stress parameters close to those of the control group (for GSH levels p< .001, for MDA levels p< .01 in the PCX+CVN group). Conclusion: According to the findings, CVN appears to preserve cochlear function in rats against the disruptive effects of PCX.
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Clinical and Experimental Health Sciences
Clinical and Experimental Health Sciences MEDICINE, RESEARCH & EXPERIMENTAL-
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