Veterinary Research Forum

Abstract Phthalate esters, such as dibutyl phthalate (DBP), are extensively utilized and human and animal exposure leads to serious toxic effects, including hepatotoxicity. In the present study the protective effects of royal jelly (RJ) on DBP-induced liver damage was investigated. A total number of 40 Wistar albino rats were randomly divided into eight groups (n = 5): control (corn oil), DBP (500 mg kg^-1), RJ (200 mg kg¹), Quercetin (QCN; 50.00 mg kg^-1), RJ (100 mg kg^-1) + DBP, RJ (200 mg kg^-1) + DBP, RJ (300 mg kg^-1) + DBP, QCN (50.00 mg kg^-1) + DBP. After 28 days of daily oral gavage treatment, animals were euthanized. The insulin resistance index, lipid profile and hepatic enzymes were measured on the collected serum samples. Moreover, oxidative and nitrosative stress biomarkers were determined in the liver. Histopathological alterations and ultimately cytochrome P450 2E1 (CYP2E1) activity was also assessed. Data obtained revealed that RJ significantly reduced the insulin resistance index and liver enzymes level in RJ-DBP groups. At the same time, RJ recovered the DBP-induced oxidative stress and restored the DBP-depleted glutathione. Moreover, RJ improved lipid profile and reduced significantly the DBP-induced hepatic CYP 2E1 activity in RJ-DBP groups. Dibutyl phthalate induced-hepatic damage such as necrosis of hepatocytes and scattered bleeding was alleviated in RJ-DBP group. Our data suggested that the administration of RJ could protect the DBP-induced hepatic functional and structural alterations. The RJ protective effects might be attributed to its antioxidant and anti-inflammatory properties and reduced CYP 2E1 activity.

Abstract Pulmonary fibrosis (PF) is a chronic interstitial lung disease with a progressive damage to the air sacs and deposition of collagen fibers in the lung tissue. The study aimed to explore the effects of Nigella sativa oil (NSO) or thymoquinone (TQ), alone or in combination with dexamethasone (DEX), on the development of bleomycin (BLM)-induced PF. Forty-two male rats were divided into seven groups: Control (CTRL); BLM, received a single dose of BLM on day 0, intratracheally; all remaining groups received BLM, as well. DEX, received DEX daily, intraperitoneally, 1 day before BLM and continued for 14 days; NSO and TQ groups, received daily NSO and TQ, respectively, 7 days before BLM and continued for 35 days; DEX + TQ, received both DEX and TQ; DEX + NSO, received both DEX and NSO. At the end, lung tissues were used for histopathological and biochemical analyses. BLM significantly increased the severity of fibrosis and inflammation compared to the CTRL. Bleomycin also significantly increased the amount of hydroxyproline, however, decreased most antioxidant enzymes in the lung tissue compared to the other groups. Group TQ + DEX significantly reduced the severity of BLM-induced PF as well as alterations in biochemical parameters, lung weight and O2 saturation. Nigella sativa oil slightly reduced BLM-induced PF, however, it caused non-significant hyperemia in lung tissue. Thymoquinone potentiated the effects of DEX on most biochemical and pathological alterations of BLM-induced lung injury much better than NSO. More studies are needed to support the use of NSO and TQ as potential protective agents against PF.

Abstract Aminoglycoside antibiotics (AGs) can cause neuromuscular blockade and paralysis of skeletal muscles. To compare the paralytic effects of selected AGs on some motor behaviors in mice, 24 male mice weighing 20.00 to 25.00 g were divided into four treatment groups. Each group was given one of four AGs (gentamicin, dihydrostreptomycin, apramycin and amikacin) at incremental doses that increased half-logarithmically compared to the therapeutic dose (16.00 mg kg^-1). Motor behavioral tests included open field test, inclined plane, horizontal bars, static rods, parallel bars and rotarod. Finally, the data were analyzed using descriptive and analytical statistics. Gentamicin and dihydrostreptomycin at 32.00 times of the therapeutic dose produced complete paralysis of the limbs, respiratory arrest, and even death in some animals. However, apramycin and amikacin did not show significant effects on skeletal muscle and motor behaviors at 32.00 times of the therapeutic dose. After administration of apramycin at 100 times of the therapeutic dose, four out of six mice (66.67%) died from respiratory depression. Amikacin at this dose did not cause animal death, although it caused some changes in motor behaviors with a significant difference in comparison with control values. Gentamicin demonstrated significantly more potent effects on motor behaviors compared to the other AGs. Overall, the order of potency was gentamicin > dihydrostreptomycin > apramycin > amikacin. High doses of AGs could impair the skeletal muscle function and disrupt motor behaviors in mice. Furthermore, the paralytic potency of selected AGs on skeletal muscle was significantly different.