Boric acid improves the behavioral, electrophysiological and histological parameters of cisplatin-induced peripheral neuropathy in rats

Yıldırım, Caner; Cevik, Sena; Yamaner, Hatice; Örkmez, Mustafa; Eronat, Omer; Bozdayı, Mehmet Akif; Erdem, Mehmet

doi:10.1016/j.jtemb.2021.126917

Cited by 2 publications

(1 citation statement)

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“…These data follow the previous studies that signified that oxidative stress is chiefly involved in the pathogenesis of cisplatin-induced optic nerve injury (Icel et al, 2018 ; Taşli et al, 2018 ). Moreover, cisplatin-induced DNA adducts may diminish antioxidant enzyme activity, including superoxide dismutase, catalase, and glutathione peroxidase (Yildirim et al, 2022 ). Pre- and co-treatment with tempol ameliorated cisplatin-induced oxidative stress, which, according to previous studies, supported the antioxidant properties of tempol (Youn et al, 2016 ; Ewees et al, 2019 ).…”

Section: Discussionmentioning

confidence: 99%

Tempol improves optic nerve histopathology and ultrastructures in cisplatin-induced optic neuropathy in rats by targeting oxidative stress—Endoplasmic reticulum stress—Autophagy signaling pathways

Alsemeh,

Hulail,

Mokhtar

et al. 2023

Front. Cell. Neurosci.

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IntroductionOptic neuropathy is an affection of the optic neurons, which ends with blindness and occurs either primarily due to direct affection of the optic nerve or secondarily as a complication of chronic diseases and/or adverse effects of their therapy. The search for novel therapeutic tools is crucial in addressing the limited therapeutic approaches for optic neuropathy. Therefore, the present study was developed to investigate the possible ameliorative effect of tempol against cisplatin-induced optic neuropathy and its underlying mechanism.MethodsForty-eight adult male albino Wistar rats were divided into four equal groups—control, tempol (TEM), cisplatin (CIS), and tempol and cisplatin combined (TEM+CIS). Optic nerve oxidative stress (MDA, SOD, and GPx), gene expression of endoplasmic reticulum stress (ATF-6, XBP-1, BIP, CHOP, and JNK), autophagy 6 (LC3, Beclin-1, and p62) markers, nerve growth factor-1, immunohistochemical expression of (LC3 and p62), histopathological, and electron microscopic examination were performed.ResultsHistopathological and ultrastructure examination validated that cisplatin caused optic neuropathy by inducing oxidative stress, upregulating ER stress markers, and downregulating autophagy markers, and NGF-1 expression. TEM + CIS showed improvement in optic nerve structure and ultrastructure along with oxidative stress, ER stress mRNA, autophagy (immunohistochemical proteins and mRNA) markers, and nerve growth factor mRNA expression.ConclusionsBased on previous findings, tempol represents a valid aid in cisplatin-induced optic neuropathy by implicating new molecular drug targets (ER stress and autophagy) for optic neuropathy therapy.

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