Royal Jelly Effect on Chronic Unpredictable Stress-Induced Pancreatic Oxidative and Endoplasmic Reticulum Stress and Insulin Secretion Impairment in Adult Male Rats

Abstract

Background: Royal jelly (RJ), secreted by nurse honeybees, possesses antioxidant properties. Studies have demonstrated that chronic stress can impair glucose metabolism, a process intricately linked to oxidative stress and endoplasmic reticulum (ER) stress induction. Consequently, this study investigated the effects of RJ on oxidative stress, apoptosis and ER stress markers, and insulin secretion from isolated pancreatic islets in rats subjected to chronic unpredictable stress (CUS).

Method: Four groups were established, comprising adult male rats: None-STR-Water, STR-Water, None-STR-RJ, and STR-RJ. Over 4 weeks, CUS was applied, and RJ was administered via oral gavage. A glucose tolerance test was conducted, and fasting blood samples were collected to analyze corticosterone, leptin, antioxidants, and malondialdehyde (MDA) plasma levels. Additionally, pancreatic oxidative stress and ER stress markers, apoptosis indicators, and insulin secretion from isolated pancreatic islets were evaluated.

Results: Exposure to CUS increased plasma corticosterone and leptin levels, catalase activity and glutathione (GSH) levels in both plasma and pancreatic tissue and reduced plasma MDA levels. RJ administration in the STR-RJ group restored the mentioned parameters. Furthermore, CUS elevated pancreatic BIP, CHOP, and cleaved CASPASE-3 protein levels; however, these levels were diminished following RJ treatment. The CALNEXIN protein level remained unchanged between the study groups. In the STR-Water group, glucose-stimulated insulin secretion was diminished, whereas in the RJ-treated groups, insulin secretion from islets in response to the high glucose concentration was significantly enhanced.

Conclusion: The administration of RJ, in conjunction with CUS exposure, may protect the normal insulin response to glucose by mitigating oxidative stress, as evidenced by the restoration of catalase activity and GSH levels, and ER stress, as supported by the decrease in BIP and CHOP protein levels.