AI Summary & Key Takeaways
AI InsightConclusion: RJ may be a potential preventive agent against the hepatic toxicity associated with cisplatin therapy.
📌 3 Key Takeaways
Abstract
To evaluate the protective effects of royal jelly (RJ) on the changes caused by cisplatin in paraoxonase-1 (PON-1) and arylesterase (ARE) activities. Materials and methods: Twenty-four Sprague-Dawley rats were divided into 4 groups of 6: control, royal jelly (300 mg kg-1 day-1, cisplatin (7 mg kg-1 body weight), and royal jelly (300 mg kg-1 day-1 plus a single dose of cisplatin (7 mg kg-1 body weight). After the experimental procedures, blood and liver tissue samples were taken from each animal. The effects of RJ and cisplatin were evaluated by PON-1, ARE (in liver homogenates), and serum alanine aminotransferase measurements. The liver tissue was also histologically examined. Results: Administration of cisplatin reduced the PON-1 and ARE activities in the liver. However, in the rats given a pretreatment with RJ before the injection of cisplatin, the reduction caused by the cisplatin in the PON-1 and ARE activities was prevented at a significant level. These biochemical observations were supported by histological findings and suggested that RJ restored the cisplatin-induced structural alterations in the liver tissue by the way of its antioxidant, radical scavenging, and antiapoptotic effects. Conclusion: RJ may be a potential preventive agent against the hepatic toxicity associated with cisplatin therapy.
Özet
To evaluate the protective effects of royal jelly (RJ) on the changes caused by cisplatin in paraoxonase-1 (PON-1) and arylesterase (ARE) activities. Materials and methods: Twenty-four Sprague-Dawley rats were divided into 4 groups of 6: control, royal jelly (300 mg kg-1 day-1, cisplatin (7 mg kg-1 body weight), and royal jelly (300 mg kg-1 day-1 plus a single dose of cisplatin (7 mg kg-1 body weight). After the experimental procedures, blood and liver tissue samples were taken from each animal. The effects of RJ and cisplatin were evaluated by PON-1, ARE (in liver homogenates), and serum alanine aminotransferase measurements. The liver tissue was also histologically examined. Results: Administration of cisplatin reduced the PON-1 and ARE activities in the liver. However, in the rats given a pretreatment with RJ before the injection of cisplatin, the reduction caused by the cisplatin in the PON-1 and ARE activities was prevented at a significant level. These biochemical observations were supported by histological findings and suggested that RJ restored the cisplatin-induced structural alterations in the liver tissue by the way of its antioxidant, radical scavenging, and antiapoptotic effects. Conclusion: RJ may be a potential preventive agent against the hepatic toxicity associated with cisplatin therapy.