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Article 2025 · 2 atıf

Carvacrol Coadministration Ameliorates Lambda-Cyhalothrin-Induced Peripheral Neuropathy in Rats: Behavioral and Molecular Evidence

Kandemir, Ozge, Ileriturk, Mustafa, Gur, Cihan, Akaras, Nurhan, Simsek, Hasan, Yilmaz, Selcuk, Kandemir, Fatih Mehmet

Özet

This study aimed to investigate the possible neuroprotective effects of Carvacrol (CRV) against Lambda-cyhalothrin (CYH)-induced peripheral neuropathy. Thirty-five rats were divided into five groups: Control, CRV, CYH, CYH+CRV25, and CYH+CRV50. CRV 25 or 50 mg/kg and CYH 6.23 mg/kg were administered orally for 21 days. The effects of these treatments were evaluated by hot plate and rotarod tests, followed by molecular, biochemical, histopathological, and immunohistochemical analyses of sciatic nerve tissues. CYH administration significantly impaired both sensory and motor functions. CRV doses (25 mg/kg and 50 mg/kg) administered with CYH significantly improved these impairments (p < 0.001). Additionally, CYH increased MDA levels and decreased antioxidants, while CRV treatment reversed these effects. CRV also suppressed inflammation (p < 0.01), apoptosis (p < 0.001), and endoplasmic reticulum stress (p < 0.001), with the 50 mg/kg dose being more effective. Morphological and immunohistochemical analyses showed that CRV treatment partially repaired CYH-induced nerve damage, with both doses reducing 8-OHdG and beclin-1 immunoreactions. The data revealed that CYH induced inflammation, oxidative stress, ER stress, and apoptosis in sciatic tissue, while CRV exhibited antioxidant, anti-inflammatory, and antiapoptotic effects, reducing the damage and suggesting its potential as a supportive treatment for CYH-induced sciatic damage.

Anahtar Kelimeler
carvacrol cyhalothrin oxidative stress peripheral neuropathy sciatic nerve OXIDATIVE STRESS GENE-EXPRESSION LIVER-INJURY INFLAMMATION INVOLVEMENT APOPTOSIS TISSUE
WoS Kategorileri
Biochemistry & Molecular Biology Toxicology
Sürdürülebilir Kalkınma Amaçları
Künye
Dergi
JOURNAL OF BIOCHEMICAL AND MOLECULAR TOXICOLOGY
Yıl
2025
Cilt
39
Sayı
7
ISSN
1095-6670
eISSN
1099-0461
DOI
10.1002/jbt.70400
WoS UID
WOS:001528990500001
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