Objective: This study aimed to explore whether carvacrol (CV) had a protective effect on paclitaxel-induced ototoxicity from biochemical, functional, and histopathological perspectives.Methods: Forty Wistar albino male rats were randomly separated into five groups of eight rats. Group 1 was the control group, so Paclitaxel or CV was not administered. Group 2 was administered i.p. CV at 25 mg/kg once a week; Group 3, was administered i.p. paclitaxel at 5 mg/kg once a week; Group 4 was administered i.p. paclitaxel at 5 mg/kg followed (30 min later) by CV at 25 mg/kg once a week; and Group 5 was administered i.p. CV at 25 mg/kg followed (1 day later) by paclitaxel at 5 mg/kg. once a week. The drugs were administered intraperitoneally once a week for four consecutive weeks, and distortion product otoacoustic emissions (DPOAE) tests were performed at the beginning of the study before the first drug administration and at the end of the study after the last drug administration. All rats were sacrificed, and cochleae were removed for biochemical and histopathological analysis. Results: Biochemical data indicated that paclitaxel caused oxidative stress in the cochlea. Histopathological findings revealed the loss of outer hair cells in the organ of Corti (CO) and moderate degenerative changes in the stria vascularis (SV). It was observed that DPOAE measurements were significantly reduced at high frequencies. In groups which CV was administered together with paclitaxel, these biochemical, histopathological, and functional changes were favorably reversed. Conclusion: CV may have a protective effect against paclitaxel-induced ototoxicity when given.
Aim Ovarian ischemia–reperfusion (I/R) injury is a serious gynecological condition that affects women of reproductive age and reduces ovarian reserve. Management of I/R injury with detorsion causes reperfusion damage, in which oxidative stress plays a central role. This study aimed to investigate whether the gossypin (GOS) with antioxidant properties, a flavonoid, has beneficial effects on the biochemical, molecular, and histopathological aspects of ovarian I/R injury. Methods Thirty‐three female Balb/c mice were randomly divided into five groups as follows: Healthy (Sham‐operated control group), I/R (IR group), I/R + GOS 5 (I/R with GOS 5 mg/kg), I/R + GOS 10 (I/R with GOS 10 mg/kg), and I/R + GOS 20 (I/R with GOS 20 mg/kg). This was followed by 3 h of ischemia and subsequent reperfusion for 3 h after detorsion was exposed. GOS was injected 2 h before reperfusion. Results IL‐1β, IL‐6, TNF‐α, NF‐κB, and CASP‐3 mRNA expressions, SOD (superoxide dismutase) activity, GSH (glutathione), and MDA (malondialdehyde) levels, and histopathological changes were evaluated in ovarian tissue. Histological examination indicated that treatment of ovarian I/R injury with GOS led to the improvement of ovarian tissue, which was accompanied by an increase in SOD activity and GSH level and a decrease in MDA level, NF‐κB, TNF‐α, IL‐1β, and IL‐6 expressions. GOS was also corrected by reducing the elevated expression of CASP‐3 as apoptosis‐change marker. Conclusion These findings indicate that the treatment of GOS may be useful as a conservative approach to reverse I/R injury via amelioration of oxidative stress parameters and histopathological scores, attenuation of inflammation, and the suppression of apoptosis.
The presence of 5-HT7r’s in both human and rat cardiovascular and immune tissues and their contribution to inflammatory conditions prompted us to hypothesize that these receptors contribute in acute myocardial infarction (MI) with underlying chronic endothelial dysfunction. We investigated the role of 5-HT7 receptors on heart tissue that damaged by isoproterenol (ISO)-induced MI in rats with high-fat diet (HFD). In vitro and in vivo effects of 5-HT7r agonist (LP44) and antagonist (SB269970) have been investigated on the H9C2 cell line and rats, respectively. For in vivo analyses, rats were fed with HFD for 8 weeks and after this period ISO-induced MI model has been applied to rat. To investigate the role of 5-HT7r’s, two different doses of LP44 and SB269970 were evaluated and compared with standard hypolipidemic agent, atorvastatin. In vitro studies showed that LP44 has protective and proliferative effects on rat cardiomyocytes. Also in in vivo studies stimulating 5-HT7r’s by LP44 improved blood lipid profile (decreased total cholesterol, low-density lipoprotein-C, and triglyceride, increased high-density lipoprotein), decreased cardiac damage markers (creatine kinase and troponin-I), and corrected inflammatory status (tumor necrosis factor-α, interleukin-6). Our results showed significant improvement in LP44 administered rats in terms of histopathologic analyses. In damaged tissues, 5-HT7 mRNA expression increased and agonist administration decreased this elevation significantly. We determined for the first time that 5-HT7r’s are overexpressed in ISO-induced MI of rats with underlying HFD-induced endothelial dysfunction. Restoration of this overexpression by LP44, a 5-HT7r agonist, ameliorated heart tissue in physiopathologic, enzymatic, and molecular level, showing the cardiac role of these receptors and suggesting them as future potential therapeutic targets.
Contrast media (CM) is known to have nephrotoxic adverse effects. Epigallocatechin-3-gallate (EGCG) is the most abundant and active catechin in green tea, and has strong antioxidant and anti-inflammatory properties. This study investigated whether EGCG can reduce contrast-induced nephrotoxicity (CIN), alone or with glycerol (GLY)-induced renal damage, and to understand its mechanisms of protection against toxicity, using models of GLY and CIN in rats. The rats were separated into eight groups (n = 6 in each), as follows: Healthy, GLY, CM, GLY + CM, CM + EGCG 50 mg/kg (po), GLY + CM + EGCG 50 mg/kg (po), CM + EGCG 100 mg/kg (po), and GLY + CM + EGCG 100 mg/kg (po). Both doses of EGCG protected against CM-induced renal dysfunction, as measured by serum creatinine and blood urea nitrogen (BUN). In addition, EGCG treatment markedly improved CIN-induced oxidative stress, and resulted in a significant down-regulatory effect on tumor necrosis factor (TNF)-α and nuclear factor (NF)-κB mRNA expression. Moreover, histopathological analysis showed that EGCG also attenuated CM-induced kidney damage. Considering the potential clinical use of CM and the numerous health benefits of EGCG, this study showed the protective role of multi-dose EGCG treatment on CIN and GLY-aggravated CIN through different mechanisms.
Amaç: Bu çalışmanın amacı, güçlü serbest radikal süpürücü ve antioksidan özelliklere sahip farnesenin paklitaksel kaynaklı ototoksisite üzerindeki etkilerini biyokimyasal ve fonksiyonel yönden araştırmaktır. Gereç ve Yöntem: On sekiz erkek Wistar albino sıçan, altı sıçandan oluşan üç gruba rastgele ayrıldı. Araştırma boyunca kontrol grubuna paklitaksel veya farnesen verilmedi. Paklitaksel grubuna, 5mg/kg paklitaksel intraperitoneal olarak dört kez (1., 7., 14. ve 21. günlerde) verildi. Farnesen + paklitaksel grubuna, önce 5 mg/kg paklitaksel, 30 dakika sonra 50 mg/kg farnesen intraperitoneal olarak 4 kez (1., 7., 14. ve 21. günlerde) verildi. 0. ve 21. günlerde tüm sıçanların otoakustik emisyon ölçümü yapıldı. Daha sonra hayvanlar sakrifiye edildi ve biyokimyasal testler için kokleaları çıkarıldı. Bulgular: Paklitaksel, önemli ölçüde malondialdehit seviyelerini yükselterek ve glutatyon seviyelerini düşürerek kokleada oksidatif strese neden oldu. Ayrıca paklitaksel grubunun distorsiyon ürünü otoakustik emisyon değerleri diğer gruplara göre anlamlı derecede düşüktü. Farnesen+paklitaksel grubunda ise paklitakselin çeşitli biyokimyasal ve fonksiyonel parametrelerde oluşturduğu hasarda iyileşmeler gözlendi. Sonuç: Çalışma sonuçları doğal bir antioksidan olan farnesen’in sıçanlarda paklitaksel kaynaklı işitme kaybını azalttığını, farnesen ve paklitaksel kombinasyonunun gelecekte klinik kullanım için paklitaksel kaynaklı ototoksisiteden koruyabileceğini göstermektedir.
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