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Article 2022 · 2 atıf

THE EFFECT OF CARVACROL UPON EXPERIMENTALLY INDUCED DIABETIC NEUROPATHY AND NEUROPATHIC PAIN IN RATS

Ekinci, Bilge, Suleyman, Bahadir, Mammadov, Renad, Gezer, Arzu, Mendil, Ali Sefa, Akbas, Nergis, Bulut, Seval, Dal, Cagatay Nusret, Suleyman, Halis

Özet

Diabetic neuropathies are the most frequent complication of diabetes. While numerous meta-bolic pathways are disrupted in diabetic neuropathy, oxidative stress has been indicated as a significant reason for this condition. In this study, the effect of carvacrol, which has antioxidant effects, on experi-mental diabetic neuropathy and neuropathic pain was investigated. Alloxan was used to induce diabetes in the experiment. Diabetes was created by administering 120 mg/kg of alloxan intraperitoneally (i.p) once a day for 3 days. Rats with a blood glucose concentration above 250 mg/kg in the blood taken from the tail veins at the end of three days were considered diabetic. Rats were categorized under healthy con-trol (HG), alloxan-induced hyperglycemia (AG), and alloxan-induced hyperglycemia + carvacrol-treated (ACG) groups. Carvacrol was i.p injected at 50 mg/kg dose to the ACG (n = 6) group of rats with hyper-glycemia. The same volume of distilled water as the solvent was applied in the same way to AG (n = 6) and HG (n = 6) rat groups. This procedure was repeated once a day for three months. Carvacrol showed an anti-hyperglycemic effect in diabetic rats, a protective effect against lowering pain threshold, and an-algesic activity in rat paws. Carvacrol prevented the oxidant/antioxidant balance from changing in favor of oxidants. The results supported that carvacrol is an agent against alloxan-induced peripheral diabetic neuropathic pain.

Anahtar Kelimeler
alloxan carvacrol diabetic neuropathy oxidative stress rats INDUCED OXIDATIVE STRESS NERVE TISSUE CELLS MODEL
WoS Kategorileri
Pharmacology & Pharmacy
Sürdürülebilir Kalkınma Amaçları
Künye
Dergi
ACTA POLONIAE PHARMACEUTICA
Yıl
2022
Cilt
79
Sayı
5
Sayfa
707-715
ISSN
0001-6837
eISSN
2353-5288
DOI
10.32383/appdr/155354
WoS UID
WOS:000925006900009
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