Comparative neuroprotective effects of royal jelly and its unique compound 10-hydroxy-2-decenoic acid on ischemia-induced inflammatory, apoptotic, epigenetic and genotoxic changes in a rat model of ischemic stroke

ABSTRACT

Objectives

This study aimed to compare the efficacy of royal jelly (RJ) and its major fatty acid 10-hydroxy-2-decenoic acid (10-HDA) on ischemic stroke-related pathologies using histological and molecular approaches.

Methods

Male rats were subjected to middle cerebral artery occlusion (MCAo) to induce ischemic stroke and were supplemented daily with either vehicle (control group), RJ or 10-HDA for 7 days starting on the day of surgery. On the eighth day, rats were sacrificed and brain tissue and blood samples were obtained to analyze brain infarct volume, DNA damage as well as apoptotic, inflammatory and epigenetic parameters.

Results

Both RJ and 10-HDA supplementation significantly reduced brain infarction and decreased weight loss when compared to control animals. These effects were associated with reduced levels of active caspase-3 and PARP-1 and increased levels of acetyl-histone H3 and H4. Although both RJ and 10-HDA treatments significantly increased acetyl-histone H3 levels, the effect of RJ was more potent than that of 10-HDA. RJ and 10-HDA supplementation also alleviated DNA damage by significantly reducing tail length, tail intensity and tail moment in brain tissue and peripheral lymphocytes, except for the RJ treatment which tended to reduce tail moment in lymphocytes without statistical significance.

Conclusions

Our findings suggest that neuroprotective effects of RJ in experimental stroke can mostly be attributed to 10-HDA.

KEYWORDS:

• Middle cerebral artery occlusion
• ischemic stroke
• royal jelly
• 10-hydroxy-2-decenoic acid
• neuroprotection
• comet
• inflammation
• apoptosis

Disclosure statement

No potential conflict of interest was reported by the author(s).

Data availability statement

The data that support the findings of this study are available from the corresponding author, [MC], upon reasonable request.

Additional information

Funding

This work was supported by the Scientific and Technological Research Council of Türkiye (TUBITAK) [grant number 118S391].

Notes on contributors

Mehmet Cansev

Mehmet Cansev is a Professor of Pharmacology at Faculty of Medicine, Bursa Uludag University, Bursa, Turkey. Dr. Cansev graduated as a medical doctor and received his doctorate in Pharmacology from Bursa Uludag University. He did his post-doctoral studies with Prof. Richard Wurtman at Massachusetts Institute of Technology (MIT) between 2004 and 2008. His research work has focused on role of phosphatide precursors in synaptogenesis and the utility of nutritional approaches in rodent models of neurodegenerative diseases. He has published more than 60 peer-reviewed papers and mentored masters and graduate students. Dr. Cansev was awarded the Best Young Pharmacologist by Turkish Pharmacological Society in 2008, Best Young Scientist by Turkish Academy of Sciences (TUBA) in 2009 and Incentive Award in Medicine by the Scientific and Technological Research Council of Turkey (TUBITAK) in 2014. Dr. Cansev is married and father to two.