The aim of this study was to evaluate potential protective effects of propolis on furan-induced hepatic damage by assessing the levels of malondialdehyde (MDA) and reduced glutathione (GSH), antioxidant enzyme activities, and histopathological changes in the liver. Albino Wistar rats were divided into six groups: a control, propolis-treated (100 mg/kg b.w./day), low-dose furan-treated (furan-L group; 2 mg/kg b.w./day), high-dose furan-treated (furan-H group; 16 mg/kg b.w./day), furan-L+propolis treated, and furan-H+propolis treated group. Propolis and furan were applied by gavage; propolis for 8 days, and furan for 20 days in furan-L groups and 10 days in furan-H groups. While MDA levels were elevated in furan-treated groups, levels of GSH and activities of antioxidant enzymes decreased (p < 0.001). The levels of MDA and GSH and activities of antioxidant enzymes were normal in the furan+propolis groups, especially in the furan-L+propolis group (p < 0.001). While the aspartate transaminase, alanine transaminase, alkaline phosphatase, and lactate pdehydrogenase activities were elevated in the furan-H treated group (p < 0.05 and p < 0.001), they were unchanged in the furan-L treated group. Histopathologically, several lesions were observed in the liver tissues of the furan-treated groups, especially in the higher-dose group. It was determined that these changes were milder in both of the furan+propolis groups. The results indicate that propolis exhibits good hepatoprotective and antioxidant potential against furan-induced hepatocellular damage in rats.

Introduction: Thyroid hormones play a major role in the regulation of testicular maturation and growth and in the control of Sertoli and Leydig cell functions in adulthood. When naturally occurring, hypothyroidism causes male hypogonadotropic hypogonadism and Sertoli cell function disorders, but when iatrogenic and methimazole-induced its influence on the pituitary-testicular axis function with respect to Sertoli cells is poorly known. Material and Methods: Male adult Wistar rats (n = 14) were divided into two groups: E – taking methimazole orally for 60 days, and C – control animals. After 60 d, the concentrations in serum of testosterone, follicle-stimulating and luteinising hormones, and inhibins A and B were measured. Testicles were examined morphologically: the apoptotic Sertoli cell percentage (ASC%) and number of these cells functional per tubular mm² (FSCN/Tmm²) were calculated. Results: In group E, inhibin A was higher while inhibin B was lower than in group C. ASC% was higher and FSCN/Tmm² lower in group E than in group C. Conclusion: A specific modulation of Sertoli cell function in the course of methimazole-induced hypothyroidism leads to a simultaneous concentration increase in inhibin A and decrease in B. Inhibin A might share responsibility for pituitary-testicular axis dysfunction and hypogonadotropic hypogonadism in this model of hypothyroidism.

Introduction: Tiletamine-xylazine-tramadol (XFM) has few side effects and can provide good sedation and analgesia. Adenosine 5’-monophosphate-activated protein kinase (AMPK) can attenuate trigeminal neuralgia. The study aimed to investigate the effects of XFM and its specific antagonist on AMPK in different regions of the brain. Material and Methods: A model of XFM in the rat was established. A total of 72 Sprague Dawley (SD) rats were randomly divided into three equally sized groups: XFM anaesthesia (M group), antagonist (W group), and XFM with antagonist interactive groups (MW group). Eighteen SD rats were in the control group and were injected intraperitoneally with saline (C group). The rats were sacrificed and the cerebral cortex, cerebellum, hippocampus, thalamus, and brain stem were immediately separated, in order to detect AMPKα mRNA expression by quantitative PCR. Results: XFM was able to increase the mRNA expression of AMPKα1 and AMPKα2 in all brain regions, and the antagonist caused the opposite effect, although the effects of XFM could not be completely reversed in some areas. Conclusion: XFM can influence the expression of AMPK in the central nervous system of the rat, which can provide a reference for the future development of anaesthetics for animals.

The oil of Juniperus communis (JC) which is among medicinal plants, has many pharmacological activities. In this study, the effects of JC oil on serum paraoxonase (PON1), pancreatic enzymes levels and lipid levels in experimental diabetic rats were investigated.Thirty-two male Wistar-Albino rats (250-300g) were used. The rats were dividedequally into four groups, control (C), diabetes (D), JC oil (J), and diabetes + JC oil (DJ). D and DJ groups wereintraperitoneally (IP) injected with 45 mg/kg streptozotocin (STZ). JC oil was administered as 200 mg/kg/21days by oral gavage in J and DJ groups.Total cholesterol (TC) and triglyceride (TG) levels were significantly decreased in the J and DJgroups when compared to C and D groups (p≤0.001). There was no difference in TG levels between D andcontrol group (p≥0.05). Lipoprotein levels were not statistically significant between any group (p≥0.05).Comparing to the control group in the diabetes and DJ groups; significant decreased amylase levels andincreased lipase levels (p≤0.001) was observed. Paraoxonase activity in D group was statistically lower thanin the other groups (p≤0.05). There is no significant difference between the C group and the Jgroup (p>0.05).PON1 level has a significant elevation in the DJ in comparison with the D group (p≤0.05). As a result, JC oil caused an increase in antioxidant PON1 enzyme level and a decrease in lipidlevels in diabetes. The data obtained are supportive that JC oil may be a potential protective effect againstdiabetes-associated complications.

Osteoarthritis, the leading cause of chronic joint pain, is studied through different animal models, but none of them is ideal in terms of reliability and translational value. In this pilot study of female rats, 3 surgical models of osteoarthritic pain, i.e., destabilization of the medial meniscus (DMM), cranial cruciate ligament transection (CCLT), and the combination of both surgical models (COMBO) and 1 chemical model [intra-articular injection of monosodium iodoacetate (MIA)] were compared for their impact on functional pain outcomes [static weight-bearing (SWB) and punctate tactile paw withdrawal threshold (PWT)] and spinal neuropeptides [substance P (SP), calcitonin gene-related peptide (CGRP), bradykinin (BK), and somatostatin (SST)]. Six rats were assigned to each model group and a sham group. Both the chemical model (MIA) and surgical COMBO model induced functional alterations in SWB and PWT, with the changes being more persistent in the surgical combination group. Both models also produced an increase in levels of pro-nociceptive and anti-nociceptive neuropeptides at different timepoints. Pain comparison with the MIA model showed the advantage of a surgical model, especially the combination of the DMM and CCLT models, whereas each surgical model alone only led to temporary functional alterations and no change in neuropeptidomics.