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Article 2021 · 55 citations

Protective Effects of Curcumin Against Paclitaxel-Induced Spinal Cord and Sciatic Nerve Injuries in Rats

Yardim, Ahmet, Kandemir, Fatih Mehmet, Comakli, Selim, Ozdemir, Selcuk, Caglayan, Cuneyt, Kucukler, Sefa, Celik, Hamit

Abstract

Paclitaxel (PTX) is an antineoplastic agent commonly used in the treatment of solid tumors and is known to cause dose-limiting peripheral neurotoxicity. This study was performed to evaluate the protective effect of curcumin (CUR) against PTX-induced spinal cord and sciatic nerve injuries in rats. The rats were administered PTX (2 mg/kg, BW) intraperitoneally for the first 5 consecutive days followed by administration of CUR (100 and 200 mg/kg, BW daily in corn oil) orally for 10 days. Our results showed that CUR significantly reduced mRNA expression levels of NF-kappa B, TNF-alpha, IL-6, iNOS and GFAP whereas caused an increase in levels of Nrf2, HO-1 and NQO1 in the spinal cord and sciatic nerve of PTX-induced rats. In addition, CUR suppressed the activation of apoptotic and autophagic pathways by increasing Bcl-2 and Bcl-xL, and decreasing p53, caspase-3, Apaf-1, LC3A, LC3B and beclin-1 mRNA expression levels. The results showed that CUR also maintained the spinal cord and sciatic nerve histological architecture and integrity by both LFB staining and H&E staining. Immunohistochemical expressions of 8-OHdG, caspase-3 and LC3B in the PTX-induced spinal cord tissue were decreased after administration of CUR. Taken together, our findings demonstrated that CUR has protective effects on PTX-induced spinal cord and sciatic nerve injuries in rats.

Keywords
Apoptosis Curcumin Inflammation Paclitaxel Peripheral neurotoxicity INDUCED PERIPHERAL NEUROPATHY INDUCED OXIDATIVE STRESS BREAST-CANCER CELLS INDUCED APOPTOSIS KAPPA-B AUTOPHAGY INHIBITION GENE-EXPRESSION DOWN-REGULATION INFLAMMATION SUPPRESSION
WoS Categories
Biochemistry & Molecular Biology Neurosciences
Sustainable Development Goals
Citation
Journal
NEUROCHEMICAL RESEARCH
Year
2021
Volume
46
Issue
2
Pages
379-395
ISSN
0364-3190
eISSN
1573-6903
DOI
10.1007/s11064-020-03174-0
WoS UID
WOS:000590260700002
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