Cardioprotective role of royal jelly in the prevention of celecoxib-mediated cardiotoxicity in adult male albino rats.

BACKGROUND: Celecoxib, a cyclooxygenase-2 selective inhibitor non-steroidal anti-inflammatory drugs, is used for the management of short- and long-term pain as well as in other inflammatory conditions. Unfortunately, its chronic use is highly associated with serious abnormal cardiovascular events. The current study was designed to explore the effect of long-term administration of celecoxib on the cardiac tissues of male albino rats. The study also examined the alleged cardioprotective effect of royal jelly. METHODS: Thirty, male albino rats were randomly divided into 3 equal groups; 10 each: (1) rats served as the control group and received no drug; (2) rats received celecoxib (50 mg/kg/day, orally), for 30 consecutive days; (3) rats received celecoxib (50 mg/kg/day, orally) plus royal jelly (300 mg/kg/day, orally) for 30 consecutive days. Sera were collected to assay cardiac enzymes and oxidant/antioxidant status. Rats were euthanatized and cardiac tissues were dissected for quantitative estimation of apoptotic genes (Bax) and anti-apoptotic gene (Bcl-2). RESULTS: Long-term celecoxib administration caused cardiotoxicity in male albino rats as manifested by significant elevation of serum levels of creatine phosphokinase (CPK), creatine kinase-MB (CK-MB), and lactate dehydrogenase (LDH), with ameliorative effects of royal jelly against celecoxib-induced cardiotoxicity as manifested by significantly decrease in serum CPK, CK-MB, and LDH levels. It also showed a significant decrease in the oxidative stress indicator malondialdehyde (MDA) levels and the bax gene. Additionally, it demonstrated significant increases in the bcl-2 gene and superoxide dismutase (SOD) levels, which contribute to its therapeutic effects against celecoxib-induced cardiotoxicity. CONCLUSION: Long-term celecoxib administration caused cardiotoxicity in male albino rats with protective effect of royal jelly being given together. It could be concluded that royal jelly may prove a useful adjunct in patients being prescribed celecoxib. TRIAL REGISTRATION: Not applicable.

Royal Jelly, A Super Food, Protects Against Celecoxib-Induced Renal Toxicity in Adult Male Albino Rats.

Background: Celecoxib is a COX-2 nonsteroidal anti-inflammatory drug (NSAID). It is widely used for the treatment of osteoarthritis, rheumatoid arthritis, and ankylosing spondylitis. Objective: This study aimed to explore the effect of long-term administration of celecoxib on kidney of male albino rats, and to study the potential effect of treatment discontinuation on such tissues. The study also examined the alleged ameliorative effect of royal jelly (RJ). Methods: Fifty, male albino rats were divided into 5 equal groups; 10 each. Group 1: rats received no drug (control group). Group 2: rats received celecoxib (50 mg/kg/day, orally for 30 successive days). Group 3: rats received celecoxib (50 mg/kg/day, orally) and royal jelly (300 mg/kg/day, orally) for 30 successive days. Group 4: rats received celecoxib for 30 successive days, then rats were left untreated for another 30 days. Group 5: rats received celecoxib and RJ for 30 successive days, then rats were left untreated for another 30 days. Results: Long-term celecoxib administration caused significant elevation in kidney function tests, with ameliorative effects of RJ against celecoxib-induced renal toxicity. Conclusion: Long-term celecoxib administration caused renal toxicity in male albino rats, with ameliorative effects of RJ.

Contexte: Le célécoxib est un anti-inflammatoire non stéroïdien (AINS) inhibiteur de COX-2. Ce médicament est largement utilisé pour le traitement symptomatique de l'arthrose, de la polyarthrite rhumatoïde et de la spondylarthrite ankylosante. Objectifs: Cet essai visait à examiner l'effet d'une administration à long terme de célécoxib sur les reins de rats albinos mâles, à étudier les possibles effets de l'arrêt du traitement sur ces tissus et à vérifier l'effet d'amélioration allégué de la gelée royale. Méthodologie: Cinquante rats albinos mâles ont été répartis en cinq groupes égaux (10 rats par groupe). Groupe 1 (groupe témoin): rats n'ayant reçu aucun médicament. Groupe 2: rats ayant reçu du célécoxib (50 mg/kg/jour, par voie orale pendant 30 jours consécutifs). Groupe 3: rats ayant reçu du célécoxib (50 mg/kg/jour, par voie orale) et de la gelée royale (300 mg/kg/jour, par voie orale) pendant 30 jours consécutifs. Groupe 4: rats ayant reçu du célécoxib pendant 30 jours consécutifs, puis laissés sans traitement pendant 30 jours supplémentaires. Groupe 5: rats ayant reçu du célécoxib et de la gelée royale pendant 30 jours consécutifs, puis laissés sans traitement pendant 30 jours supplémentaires. Résultats: L'administration à long terme de célécoxib a entraîné une augmentation significative des tests de la fonction rénale; la gelée royale a montré des effets d'amélioration contre la toxicité rénale induite par le célécoxib. Conclusion: L'administration à long terme de célécoxib a provoqué une toxicité rénale chez les rats albinos mâles contre laquelle la gelée royale a montré des effets protecteurs.

Di (2-ethylhexyl) phthalate alters neurobehavioral responses and oxidative status, architecture, and GFAP and BDNF signaling in juvenile rat's brain: Protective role of Coenzyme10.

Di-(2-ethylhexyl) phthalate (DEHP), a phthalate plasticizer, is widely spread in the environment, presenting hazards to human health and food safety. Hence, this study examined the probable preventive role of coenzyme10 (CQ10) (10 mg/kg.b.wt) against DEHP (500 mg/kg.wt) - induced neurotoxic and neurobehavioral impacts in juvenile (34 ± 1.01g and 3 weeks old) male Sprague Dawley rats in 35-days oral dosing trial. The results indicated that CQ10 significantly protected against DEHP-induced memory impairment, anxiety, depression, spatial learning disorders, and repetitive/stereotypic-like behavior. Besides, the DEHP-induced depletion in dopamine and gamma amino butyric acid levels was significantly restored by CQ10. Moreover, CQ10 significantly protected against the exhaustion of CAT, GPx, SOD, GSH, and GSH/GSSG ratio, as well as the increase in malondialdehyde, Caspas-3, interleukin-6, and tumor necrosis factor-alpha brain content accompanying with DEHP exposure. Furthermore, CQ10 significantly protected the brain from the DEHP-induced neurodegenerative alterations. Also, the increased immunoexpression of brain-derived neurotrophic factor, not glial fibrillary acidic protein, in the cerebral, hippocampal, and cerebellar brain tissues due to DEHP exposure was alleviated with CQ10. This study's findings provide conclusive evidence that CQ10 has the potential to be used as an efficient natural protective agent against the neurobehavioral and neurotoxic consequences of DEHP.

Bee venom (Apis mellifera L.) rescues zinc oxide nanoparticles induced neurobehavioral and neurotoxic impact via controlling neurofilament and GAP-43 in rat brain.

This study investigated the possible beneficial role of the bee venom (BV, Apis mellifera L.) against zinc oxide nanoparticles (ZNPs)-induced neurobehavioral and neurotoxic impacts in rats. Fifty male Sprague Dawley rats were alienated into five groups. Three groups were intraperitoneally injected distilled water (C 28D group), ZNPs (100 mg/kg b.wt) (ZNPs group), or ZNPs (100 mg/kg.wt) and BV (1 mg/ kg.bwt) (ZNPs + BV group) for 28 days. One group was intraperitoneally injected with 1 mL of distilled water for 56 days (C 56D group). The last group was intraperitoneally injected with ZNPs for 28 days, then BV for another 28 days at the same earlier doses and duration (ZNPs/BV group). Depression, anxiety, locomotor activity, spatial learning, and memory were evaluated using the forced swimming test, elevated plus maze, open field test, and Morris water maze test, respectively. The brain contents of dopamine, serotonin, total antioxidant capacity (TAC), malondialdehyde (MDA), and Zn were estimated. The histopathological changes and immunoexpressions of neurofilament and GAP-43 protein in the brain tissues were followed. The results displayed that BV significantly decreased the ZNPs-induced depression, anxiety, memory impairment, and spatial learning disorders. Moreover, the ZNPs-induced increment in serotonin and dopamine levels and Zn content was significantly suppressed by BV. Besides, BV significantly restored the depleted TAC but minimized the augmented MDA brain content associated with ZNPs exposure. Likewise, the neurodegenerative changes induced by ZNPs were significantly abolished by BV. Also, the increased neurofilament and GAP-43 immunoexpression due to ZNPs exposure were alleviated with BV. Of note, BV achieved better results in the ZNPs + BV group than in the ZNPs/BV group. Conclusively, these results demonstrated that BV could be employed as a biologically effective therapy to mitigate the neurotoxic and neurobehavioral effects of ZNPs, particularly when used during ZNPs exposure.