The College of Pharmacy discussed the MSc thesis entitled “Effects of Apigenin in Cisplatin-Induced Duodenal Mucositis in Comparison with Vitamin E in Rats” by the student Ayah Raafat AbdulRazzaq and the supervisor, Professor Dr. Nada Naji Alshawi, at the Pharmacology and Toxicology Department.
The study aimed to evaluate the protective and therapeutic effects of apigenin against cisplatin-induced duodenal mucositis in rats and to compare its efficacy with Vitamin E.
The study included thirty-five male rats randomly divided into five groups of seven and treated as follows: Group I rats received normal saline orally for ten consecutive days; Group II rats received normal saline orally for ten consecutive days and a single intraperitoneal (IP) injection of cisplatin at a dose of 7 mg/kg on day ten; Group III rats received apigenin at a dose of 5 mg/kg orally for ten consecutive days and a single IP injection of cisplatin at a dose of 7 mg/kg on day ten; Group IV rats received apigenin at a dose of 10 mg/kg orally for ten consecutive days and a single IP injection of cisplatin at a dose of 7 mg/kg on day ten; Group V received Vitamin E at a dose of 100 mg/kg orally for ten consecutive days and a single IP injection of cisplatin at a dose of 7 mg/kg on day ten. Subsequently, the rats were sacrificed, and blood and duodenal tissue samples were collected for biochemical, gene expression, and histological analysis.
The results showed that apigenin treatment significantly improved the histopathological alterations induced by cisplatin in the duodenal tissue, and reduced oxidative stress by increasing GSH and decreasing MDA levels compared to Group II. Furthermore, apigenin decreased the expression of inflammatory markers, including TNF-α and IL-13, and reduced the apoptotic marker caspase-3 levels, with greater efficacy than Vitamin E across several parameters.
The study recommended conducting further experimental and clinical investigations to evaluate the therapeutic potential of apigenin and its possible use as a protective agent against cisplatin-induced gastrointestinal toxicity.
