Kurşun asetat maruziyetine bağlı gelişen mide hasarında naringinin visfatin ve TNF-α immunreaktivitesi üzerinden potansiyel koruyucu etkilerinin belirlenmesi

Abstract

Amaç: Bu çalışma, güçlü antioksidan ve antiinflamatuvar özelliklere sahip doğal bir flavonoid olan naringinin, kurşun asetatın neden olduğu gastrik mukozal hasara karşı koruyucu etkilerini araştırmayı amaçlamıştır. Kurşun toksisitesi, mide mukozasında oksidatif stres ve inflamatuvar yanıtı artırarak morfolojik bütünlüğü bozmaktadır. Bu nedenle, naringinin bu patolojik süreç üzerindeki potansiyel düzenleyici rolü değerlendirilmiştir. Yöntem: Toplam 28 erkek Wistar albino sıçan dört gruba ayrılmıştır: kontrol, naringin (40 mg/kg), kurşun asetat (500 ppm) ve kurşun asetat+naringin. Uygulamalar 30 gün boyunca orogastrik gavaj ve içme suyu yoluyla gerçekleştirilmiştir. Deney sonunda elde edilen mide dokuları Hematoksilen–Eozin (H&E) boyası ile histopatolojik olarak, visfatin ve TNF-α antikorları kullanılarak immünohistokimyasal olarak değerlendirilmiştir. Bulgular: Kurşun asetat uygulaması, belirgin ödem, epitel dejenerasyonu, muskularis mukozaya kadar uzanan erozyon, vasküler konjesyon ve yoğun inflamatuvar infiltrasyona neden olmuştur (p<0.001). Buna karşın, naringin tedavisi bu hasar parametrelerinde anlamlı azalma sağlamış, mide mukozasının histolojik bütünlüğünü korumuştur. Ayrıca, kurşun asetat grubunda artan visfatin ve TNF-α immünreaktivitesi, naringin uygulamasıyla belirgin biçimde azalmıştır (p<0.05). Sonuç: Naringin, kurşun asetatın neden olduğu gastrik mukozal hasarı yapısal bütünlüğü koruyarak ve inflamatuvar yanıtı baskılayarak önlemiştir. Bulgular, naringinin inflamatuvar yanıtla ilişkili belirteçler üzerindeki düzenleyici etkileri ve histolojik bulgular ışığında, gastrik doku bütünlüğünün korunmasına katkı sağlayabileceğini düşündürmektedir. Naringin, ağır metal kaynaklı gastrointestinal toksisitelerde koruyucu veya tamamlayıcı bir farmakolojik ajan olarak değerlendirilebilir.

Keywords

• Naringin
• Kurşun asetat
• Gastrik mukozal hasar
• Visfatin
• TNF-α

Determination of the potential protective effects of naringin on lead acetate–induced gastric injury through visfatin and TNF-α immunoreactivity

Abstract

Aim: This study aimed to investigate the protective potential of naringin, a natural flavonoid with potent antioxidant and anti-inflammatory properties, against lead acetate-induced gastric mucosal injury in rats. Lead toxicity disrupts gastric morphology through oxidative stress and excessive inflammatory activation. Therefore, the present research evaluated whether naringin could preserve gastric integrity by modulating inflammation and cellular stress responses. Method: Twenty-eight adult male Wistar albino rats were randomly divided into four groups: control, naringin (40 mg/kg), lead acetate (500 ppm), and lead acetate+naringin. Treatments were administered for 30 consecutive days by oral gavage and in drinking water. At the end of the experiment, gastric tissues were collected for histopathological examination using Hematoxylin–Eosin staining and for immunohistochemical assessment of visfatin and TNF-α expression. Results: Lead acetate exposure caused severe gastric mucosal alterations, including edema, epithelial cell degeneration, erosion extending to the muscularis mucosa, vascular congestion, and intense inflammatory cell infiltration (p<0.001). In contrast, naringin treatment significantly alleviated these pathological changes, maintaining tissue morphology close to that of the control group. Moreover, visfatin and TNF-α immunoreactivity levels were markedly increased in the lead acetate group but significantly decreased in the lead acetate+naringin group (p<0.05), indicating a strong anti-inflammatory response. Conclusion: Naringin demonstrated significant gastroprotective effects against lead-induced mucosal injury by preserving histological integrity and suppressing pro-inflammatory cytokine expression. The findings suggest that naringin may help preserve gastric tissue integrity by regulating inflammatory markers and may be considered a protective or adjunctive agent in heavy metal–induced gastrointestinal toxicities.

Keywords

• Naringin
• Lead acetate
• Gastric mucosal injury
• Visfatin
• TNF-α

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