Propolis is a natural resinous substance produced by honeybees that has many biological activities. For thousands of years, it has been widely used as a dietary supplement and traditional medicine to treat a variety of ailments due to its antimicrobial, anti-inflammatory, antioxidant, immunomodulatory, and wound-healing properties. Nutritional supplements and foods may interact with drugs both pharmacodynamically and pharmacokinetically, which could raise clinical concerns. Background/Objectives: This study aimed to investigate the effect of propolis on the plasma disposition of enrofloxacin and to assess the potential pharmacokinetic interaction in rabbits. Methods: In this study, enrofloxacin was applied per os (20 mg/kg) and IM (10 mg/kg) and with propolis (100 mg resin/kg) administration in four groups of rabbits (each of six individuals). Heparinized blood samples were collected at 0, 0.1, 0.3, 0.5, 1, 2, 4, 8, 12, and 24 h post-administration. HPLC-FL was used to analyze the plasma concentrations of enrofloxacin and its active metabolite ciprofloxacin following liquid–liquid phase extraction, i.e., protein precipitation with acetonitrile and partitioning with sodium sulfate. Results: The results revealed that propolis coadministration significantly affected the plasma disposition of enrofloxacin and its active metabolite after both per os and intramuscular administration routes. Significantly greater AUC (48.91 ± 11.53 vs. 26.11 ± 12.44 µg.h/mL), as well as longer T_1/2λz (11.75 ± 3.20 vs. 5.93 ± 2.51 h) and MRT (17.26 ± 4.55 vs. 8.96 ± 3.82 h) values of enrofloxacin and its metabolite ciprofloxacin, were observed after the coadministration of propolis compared to enrofloxacin alone following both per os and IM routes in rabbits. Conclusions: The concurrent use of propolis and prescription medications may prolong the half-life (T_1/2λz) and increase the systemic availability of chronically used drugs with narrow therapeutic indices. The repeated use of drugs such as antibiotics, heart medications, and antidepressants, or drugs with a narrow therapeutic index such as antineoplastic and anticoagulant agents, can cause toxic effects by raising blood plasma levels. Considering the varied metabolism of rabbits and humans, further validation of this study may require thorough clinical trials in humans.

Cisplatin is a potent chemotherapeutic agent whose clinical application is frequently limited by severe nephrotoxicity. N-acetylserotonin (NAS), a precursor of melatonin and a selective agonist of the TrkB receptor, has demonstrated significant antioxidant and neuroprotective properties. This study aimed to evaluate the potential renoprotective effects of NAS against cisplatin-induced acute kidney injury (AKI) in a rat model. Thirty-five Wistar Albino rats were divided into five groups: Control, Sham, NAS (5 mg/kg), Cisplatin (CP; 7.5 mg/kg), and CP + NAS. NAS was administered daily for seven days, while cisplatin was given as a single dose on the fourth day. Renal function was assessed via serum urea and creatinine. Oxidative stress markers, including Malondialdehyde (MDA), Superoxide Dismutase (SOD), Total Antioxidant Status (TAS), and Total Oxidant Status (TOS), were measured in kidney tissue. Comprehensive histopathological evaluations were performed to assess tubular and glomerular damage. Cisplatin administration significantly increased serum creatinine levels and induced severe histopathological damage (p < 0.05). While cisplatin reduced SOD and TAS levels, NAS treatment showed a trend toward biochemical recovery without reaching statistical significance in oxidative markers. Notably, NAS administration significantly ameliorated cisplatin-induced histopathological lesions, specifically reducing tubular epithelial loss, glomerular degeneration, interstitial inflammation, and vacuolization (p < 0.05). Our findings indicate that NAS exerts a profound structural protective effect against cisplatin-induced renal injury. The preservation of renal parenchyma, despite modest systemic biochemical shifts, suggests that NAS-mediated protection may involve localized TrkB-dependent pro-survival signaling and stabilization of mitochondrial integrity. NAS represents a promising therapeutic candidate for mitigating chemotherapy-induced nephrotoxicity.

Animal poison control centers receive numerous complaints about possible consumption of substances that can cause deadly toxicities in the home. In recent years, over-the-counter medications such as ibuprofen, acetaminophen, and herbal supplements are the most common toxic substances consumed by pets. Removal of the toxin and supportive treatment is recommended in case of exposure to a toxin that does not have a known antidote. There have been many studies in both human and veterinary medicine that supporting the use of intravenous lipid emulsions in the treatment of intoxications. Intravenous lipid emulsion (ILE) is an oil-in-water emulsion that consists of egg yolk phospholipids, water, glycerin and various oils such as soybean, fish, coconut and olive oil. It is defined as a microemulsion with a long history of use as a parenteral nutrition formulation in both adult and pediatric patients. Also used as a drug carrier in addition to parenteral nutrition. In recent years, it has been used as an effective antidote for the treatment of intoxications caused by compounds with high oil solubility in both human and veterinary medicine. The first efficacy of the use of intravenous lipid emulsions in treatments was demonstrated in the systemic toxicity of local anesthetics and nowadays it comes to the fore in the poisoning of various drugs and compounds. However, it can also be used as an antidote in various intoxication cases caused by different chemicals that do not have any known antidote. Although clinically positive responses are received, more research is needed to more clearly understand the effect of intravenous lipid emulsion.