Veterinary Research Forum

Abstract Micromeria congesta (MC) is a medicinal plant traditionally used in the Şanlıurfa, Adıyaman, and Gaziantep provinces of Türkiye for treating respiratory disorders. Despite its ethnobotanical relevance, its pharmacological effects on lung inflammation remain unclear. This study evaluated the protective effects of MC essential oil (MCEO) against lipopolysaccharide (LPS)-induced acute lung injury in rats, with a focus on inflammation and tissue damage. The MC was collected from its natural habitat, and its EO was extracted by hydro-distillation using a Clevenger-type apparatus. The Gas chromatography-mass spectrometry analysis revealed 28 compounds, with piperitenone oxide (33.97%) and pulegone (22.30%) as the main constituents. Thirty-six Wistar albino rats were randomly assigned into six groups, including three MCEO-treated (12.50, 25.00, and 50.00 mg kg^-1), dexamethasone, LPS-only, and control groups. The MCEO was administered by gavage for seven days, followed by intra-venous LPS on day eight (except for the control group). Blood and lung tissues were collected 6 hr later for biochemical, histopathological, and molecular analyses. The MCEO treatment significantly lowered blood glucose and urea levels compared to the LPS group. It also modulated NLRP3, caspase-3, and tumor necrosis factor alpha genes expressions, as determined by RT-PCR analysis, indicating anti-inflammatory effects. Histopathological findings confirmed a dose-dependent reduction in lung inflammation and tissue damage. The MCEO administration alleviated LPS-induced acute lung injury in rats through anti-inflammatory and protective effects, as confirmed by molecular (NLRP3, caspase-3, and tumor necrosis factor alpha) and histopathological analyses. Additionally, MCEO reduced blood glucose and urea levels, supporting its systemic protective role against endotoxin-induced inflammation.

Abstract The present study was conducted to evaluate the effects of different doses of haloperidol (HP) on induction of oxidative stress in blood and liver cell degeneration in comparison with influences of HP pre-treatment on inflammatory process induced by intraperitoneal (IP) administration of lipopolysaccharide (LPS). One hundred twenty male albino Wistar rats were randomly divided into eight groups (15 in each), including: Control group, LPS group, three groups as HP administration in three divided doses (0.50, 1.00 and 2.00 mg kg^-1), and three treatment groups that HP was administered in three doses (0.50, 1.00 and 2.00 mg kg^-1) prior to LPS administration.Concentrations of malondialdehyde, activities of antioxidant enzymes including glutathione peroxidase, superoxide dismutase and also the levels of tumor necrosis factor-alpha and interleukin 1-beta were measured in blood and serum. In addition to liver histopathological changes evaluation, hepatic silent information regulator of transcription 1 (SIRT1) and phosphorylated-nuclear factor-κB (p-NF-κB) levels were quantitated. Our findings indicated that sole administration of HP (particularly higher doses) can induce oxidative stress in blood and cell degeneration in liver, while it can attenuate inflammatory process induced by LPS administration presumably via SIRT1 up-regulation and preventing the induction of p-NF-κB. The oxidative and degenerative effects of HP and its impact on inflammatory status were completely dose- dependent according to our results. The possible anti-inflammatory effects of HP may affect reparative mechanisms and hepatic cell degeneration. However, the influences of HP on immune system need further investigations and its higher doses should be administered cautiously especially in patients with immune system dysfunctions.

Abstract The present study aimed to examine the effectiveness of silymarin compared to hydrocortisone on clinical and hematological alterations and organ injury (liver and heart) in a low-dose canine lipopolysaccharide (LPS)-induced sepsis model. Fifteen clinically healthy dogs were randomly categorized into three equal groups: Two dogs in group A, LPS (0.10 μg kg^-1, IV) was injected (control, n = 5); Group B was similar to group A, with the difference that silymarin bolus (10.00 mg kg^-1, IV, once) was injected 40 min after LPS injection. Group C was similar to group B with the difference that hydrocortisone bolus (2.00 mg kg^-1, IV, once) was administrated instead of silymarin. Five mL of blood was collected at baseline, 1, 3, and 6 hr of the study. Septic control dogs experienced a significant reduction in red blood cells count (RBC), hemoglobin (Hb), and hematocrit (HCT) and a significant elevation in serum activities of aspartate aminotransferase (AST), alkaline phosphatase (ALP), lactate dehydrogenase (LDH), creatine kinase isoenzyme MB (CK-MB), and plasma cardiac troponin I (cTnI) concentration. We noticed a significant increase in RBCs, Hb, and HCT, and a significant decrease in AST, ALP, LDH, CK-MB, and cTnI in the silymarin group in comparison with hydrocortisone and control group. Our results suggested that silymarin had a positive influence on sepsis due to protecting RBCs, and decreasing organ (heart and liver) injury. These findings supported the hypothesis that silymarin could be more effective than routine corticosteroid therapy in sepsis.

Abstract Neuro-immune mediators play an important role in the development of sickness behaviors. In the present study, the effect of captopril on sickness behaviors caused by lipopolysaccharide (LPS) was studied in the rats. The animals were randomized into the following groups: control, sham, 10 mg kg^-1 captopril - LPS (Capto 10-LPS), 50 mg kg^-1 captopril - LPS (Capto 50-LPS), and 100 mg kg^-1 captopril - LPS (Capto 100-LPS). Behavioral tests including open-field (OF), elevated plus maze (EPM) and forced swimming (FS) test were performed, and the serum level of interleukin-6 (IL-6) was assessed. In OF, the number of crossings in the central zone in Capto 10-LPS, Capto 50-LPS, and Capto 100-LPS groups was higher than that of the sham group. In EPM, the open arm entry numbers in the sham group were lower compared to the control group. Furthermore, pretreatment by captopril increased the entries to the open arms. In FS test, the immobility time of the sham group was longer than that of the control group. In Capto 10-LPS, Capto 50-LPS, and Capto 100-LPS groups, immobility was shorter compared to the sham group. In addition, the IL-6 level was higher in the sham group compared to the control group, and treatment with 50 and 100 mg kg^-1 of captopril restored the IL-6 level in comparison with the sham group. Results confirmed that pretreatment with captopril ameliorated LPS-caused sickness behaviors and attenuated IL-6 as an inflammatory marker in the rats.

Abstract In the present study the protective effect of Nigella sativa (N. sativa)on synaptic plasticity impairment induced by lipopolysaccharide (LPS) in rats was investigated. Fifty-eight rats were grouped and treated as follows: 1) control (saline), 2) LPS, 3) LPS-N. sativa,and 4) N. sativa. In a Morris water maze test, the escape latency and traveled path to find the platform as well as time spent and the traveled distance in target quadrant (Q₁) were measured. Long term potentiation (LTP) from CA₁ area of hippocampus followed by high frequency stimulation to Schafer collateral was studied and slope, slope 10-90% and amplitude of field excitatory field potential (fEPSP) were calculated. The escape latency and traveled path in LPS group were significantly higher than those in the control group while, in LPS-N. sativa group these parameters were significantly lower than those in LPS group. The rats in LPS group spent less time and traveled shorter distance in Q₁ than the rats in the control group while, in LPS-N. sativa group the rats spent more time and traveled longer distance than the rats in LPS group. LPS significantly decreased slope, slope 10-90% and amplitude of fEPSP while, in LPS-N. sativa group these parameters increased compared to LPS group. The results indicated that the hydro-alcohol extract of N. sativa protected against synaptic plasticity and spatial learning and memory impairment induced by LPS in rats.

Abstract The present study investigated the effects of E. coli lipopolysaccharide (LPS) induced mastitis model in rat on the activity of antioxidant enzyme systems. To achieve this purpose, E. coli LPS were infused into the mammary gland of 12 rats 72 hr postpartum and compared with 12 rats in control group infused intramammary placebo sterile pyrogene – free, physiological saline. The antioxidant activities of the enzymes, superoxide dismutase, glutathione peroxidase, and catalase together with ‎‏malondialdehyde (MDA) level were assayed in blood serum, milk and mammary tissue. Results obtained showed that, the antioxidant enzyme activities in milk, blood serum and mammary tissue were significantly decreased while the level of MDA, the indicator of lipid peroxidation were significantly increased following intramammary inoculation of LPS compared to the control animals. Histopathological examination also revealed the infiltration of inflammatory cells in mammary tissue and disruption of acinar structure and acinar lumina in mastitic rats. The results indicated that LPS-induced ‎mastitis could alter antioxidant enzymes and increase lipid peroxidation.