Zingerone protects liver and kidney tissues by preventing oxidative stress, inflammation, and apoptosis in methotrexate-treated rats.

The clinical use of drugs used in the treatment of diseases is limited due to the toxic side effects, and many studies have been conducted to benefit from herbal adjuvant therapies recently to eliminate these effects. In this study, the protective effect of zingerone against liver and kidney damage generated in rats through methotrexate (MTX). Histopathological investigations were performed to determine tissue damage caused by MTX and the healing effect of zingone and liver function markers such as serum alanine transaminase (ALT), aspartate transaminase (AST), alkaline phosphatase (ALP), and renal function markers such as urea, creatine, and aquaporin-1 (AQP-1) were measured. The effects of MTX and protective properties of zingerone on oxidative stress were investigated through the measurement of malondialdehyde and reduced glutathione (GSH) levels, catalase (CAT), and glutathione peroxidase (GPx) enzyme activities. The anti-inflammatory effect of zingerone was determined by measuring the cytokine levels causing inflammation such as nuclear factor-kappa B (NF-κB), tumor necrosis factor-α (TNF-α), and interleukin-1ß (IL-1ß), and its effects on apoptosis were determined by immunohistochemical analysis of caspase-3 and B-cell lymphoma-2 (Bcl-2) expression levels. According to the results obtained within the scope of the study, it was determined that zingerone treatment prevented the increase in MTX-induced liver and kidney function markers, showed healing effects on antioxidant parameters degraded in both tissues, and decreased the inflammation parameters. It was determined that it also prevented apoptosis and possessed a protective effect on disrupted tissue architecture by decreasing the increased caspase-3 expression and increasing the decreased Bcl-2 level.

The use of inflammatory markers as a diagnostic and prognostic approach in neonatal calves with septicaemia.

The objective of this study was to evaluate the usefulness of inflammatory markers as a diagnostic and prognostic approach in neonatal calves with septicaemia. The study material consisted of 13 neonatal calves with septicaemia (septicaemic calves, SC) and ten healthy neonatal calves (control calves, CC). Blood samples were collected for biochemical, haematological and microbiological analyses. In addition, faecal samples were collected for microbiological and virological analyses. Three of neonatal calves with septicaemia were positive for E. coli (E. coli O157 serotype) by microbiological examination, but all neonatal calves with septicaemia were negative for rota- and coronaviruses. By haematological examination, there were no significant differences between SC and CC for white blood cell (WBC) and neutrophil (NEU) counts (P > 0.05). NEU counts were higher on day 0 than on day 15 in SC (P < 0.05). Red blood cell (RBC) counts and packed cell volume (PCV) values were higher on day 0 in the SC than in the CC (P < 0.05). By biochemical analyses, tumour necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), procalcitonin (PCT), haptoglobin (Hp), and fibrinogen (Fb) concentrations were higher on day 0 in the SC than in the CC (P < 0.05). After treatment (on day 15), the serum IL-6, PCT, Hp, and Fb concentrations were significantly decreased in the SC compared to the CC (P < 0.05). The serum iron (Fe) concentrations were lower on day 0 in the SC than in the CC (P < 0.05), and were higher on day 15 than on day 0 in the SC (P < 0.05). The study revealed that inflammatory markers could be used for determining the diagnosis and prognosis in neonatal calves with septicaemia.

Investigation of the effects of hesperidin and chrysin on renal injury induced by colistin in rats.

This study aimed to investigate whether hesperidin and chrysin antioxidants have protective effects on renal injury induced by colistin in rats. Renal lipid peroxidation, total glutathione (GSH) levels, superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) enzyme activities, serum urea and creatinine levels, as well as tumour necrosis factor-α (TNF-α), interleukin-6 (IL-6) and interleukin-1ß (IL-1ß) levels were determined. Injuries to the proximal and distal tubules were determined using histopathological and double immunohistochemistry examinations. The results showed that hesperidin and chrysin significantly decreased the levels of MDA and inflammatory parameters and significantly increased GSH, SOD, CAT, and GSH-Px levels against colistin-induced renal injury. The results also showed that cystatin C and calbindin D28K immunopositivities significantly increased through hesperidin and chrysin treatment. Hesperidin and chrysin alleviated the renal injury induced by colistin via anti-oxidant and anti-inflammatory activities. Thus, hesperidin and chrysin could attenuate colistin-induced nephrotoxicity via antioxidant and anti-inflammatory activities. Addition of hesperidin or chrysin to the treatment protocol of colistin treatment might benefit patient treatment in terms of the prevention of colistin-induced renal injury.

Evaluation of arginase activity, nitric oxide and oxidative stress status in sheep with contagious agalactia.

It is known that inflammatory organ damages due to various agents, such as microorganisms including mycoplasmas, lead to oxidative stress. Nitric oxide (NO) functions as an antimicrobial agent, and arginase decreases proinflammatory cytokine release. There are very few studies on arginase activity, NO level and oxidative stress status in mycoplasmal infections. Therefore, the aim of this study was to evaluate erythrocyte arginase activity, plasma NO level and oxidative stress status in sheep with contagious agalactia. The study material consisted of 10 healthy sheep and 14 sheep with contagious agalactia characterised by mastitis, arthritis and keratoconjunctivitis. Erythrocyte arginase activity, plasma NO, malondialdehyde (MDA), total oxidant capacity (TOC) and total antioxidant capacity (TAC) levels were measured. Significant decreases in erythrocyte arginase activity and plasma TAC level (P < 0.001), and significant increases in plasma NO, MDA and TOC levels (P < 0.001) were found in the diseased sheep as compared with the healthy animals. This study suggests that contagious agalactia may cause oxidative stress due to increased plasma MDA and TOC levels and decreased plasma TAC levels, and that the decrease in erythrocyte arginase activity and increase in plasma NO level may contribute to the elimination of mycoplasmal agents causing contagious agalactia.

Evaluation of Oxidative Stress in Sheep Infected with Psoroptes Ovis using Total Antioxidant Capacity, Total Oxidant Status, and Malondialdehyde Level.

INTRODUCTION: The study aimed at evaluating oxidative stress using malondialdehyde (MDA), total antioxidant capacity (TAC), total oxidant status (TOS), and oxidative stress index (OSI) markers in sheep naturally infected with Psoroptes ovis(Acari). MATERIAL AND METHODS: The study was performed on 40 sheep divided into two equal groups: a healthy group (group I) and a group naturally infected with Psoroptes ovis (group II). The sera were obtained by centrifuging blood samples collected from the vena jugularis and serum MDA level changes in the samples were measured spectrophotometrically. Commercially available test kits were used for the measurement of TAC and TOS levels. The percentage ratio of TOS level to TAC level was accepted as OSI. RESULTS: The serum malondialdehyde, total oxidant status levels, and oxidative stress index increased significantly (P < 0.01) in group II, while the serum total antioxidant capacity levels decreased significantly (P < 0.01) in this group. Negative correlations between total antioxidant capacity and total oxidant status and total antioxidant capacity and malondialdehyde, and a positive correlation between total oxidant status and malondialdehyde were found in infected sheep. CONCLUSION: The obtained results indicated the relationship between oxidant/antioxidant imbalance and Psoroptes ovis infection in sheep. Their MDA, TAC, TOS, and OSI markers may be used to determine the oxidative stress in natural infections with Psoroptes ovis.

Molecular detection of tick-borne rickettsial and protozoan pathogens in domestic dogs from Turkey.

BACKGROUND: Canine tick-borne parasites have emerged in recent years, showing a wider geographic distribution and increased global prevalence. In addition to their veterinary importance, domestic dogs play an important role in the transmission cycles of some agents by acting as reservoirs and sentinels. This study investigated Babesia, Theileria, Anaplasma, and Ehrlichia species in asymptomatic dogs in ten provinces of Turkey. METHODS: DNA obtained from blood samples collected from 757 domestic dogs (243 stray, 351 shelter, 163 pet) of both sexes and various ages were evaluated using PCR and reverse line blotting (RLB) assays. RESULTS: Of the 757 dogs tested, 41 (5.4%) were found to be infected with one or more parasites. Ehrlichia canis (37/757, 4.9%) was the most common canine tick-borne pathogen, followed by Anaplasma platys (4/757, 0.5%). Babesia canis and Theileria annulata were each detected in 1 (0.13%) sample. Combined infection of E. canis and A. platys was detected in 2 (0.3%) samples. The prevalence of tick-borne pathogens was higher in adult dogs (6.8%) than in those under one year old (3.1%). Difference in infection rate of male and female dogs was not significant. Pet dogs had a lower prevalence of infection (1.2%) compared to stray (7.4%) and shelter dogs (6%) although the difference between stray and shelter dogs was not significant. CONCLUSIONS: Babesia canis, T. annulata, A. platys, and E. canis species were identified at the molecular level in dogs in several provinces of Turkey, with E. canis being the most common species among tick-borne pathogens. Detailed studies should be conducted regarding the existence and prevalence of B. canis and Dermacentor reticulatus in eastern Turkey.

A molecular and parasitological survey of Hepatozoon canis in domestic dogs in Turkey.

In this study, asymptomatic dogs in nine provinces of Turkey were surveyed to investigate the prevalence and intensity of Hepatozoon canis infection. DNA obtained from blood samples collected from 694 domestic dogs (243 stray, 288 shelter, and 163 pets) of both genders and varying ages were evaluated by polymerase chain reaction (PCR). In addition, 285 thin blood smears prepared from these blood samples were also evaluated for microscopic examination. Direct microscopy revealed Hepatozoon gamonts in the peripheral blood of three of 285 (1.0%; 95% confidence interval (CI): 0.21-3.04) tested. Using PCR, 155 of the 694 (22.3%; 95% CI: 19.28-25.61) were found to be positive for the presence of H. canis DNA. The prevalence of infection was higher in adult dogs (26.2%; 95% CI: 22.1-30.7) than young animals (16.4%; 95% CI: 12.2-21.3). Although the prevalence determined by PCR was higher in male dogs (24.5%; 95% CI: 19.6-29.9) than in female dogs (20.8%; 95% CI: 16.9-25.1), gender differences were not significant. Pet dogs had a lower prevalence of infection (10.4%; 95% CI: 6.2-16.2) compared to stray (26.3%; 95% CI: 20.9-32.3) and shelter dogs (25.7%; 95% CI: 20.7-31.1), but no significant association between stray and shelter dogs was found for the presence of the parasite. Partial sequences of the 18S ribosomal RNA (rRNA) gene shared 99-100% similarity with the corresponding H. canis isolates. This epidemiological survey revealed a high prevalence of H. canis in dogs from several provinces in Turkey, and it suggests that the age and origin are associated with the parasite.

Rutin attenuates gentamicin-induced renal damage by reducing oxidative stress, inflammation, apoptosis, and autophagy in rats.

Gentamicin is commonly used against gram-negative microorganisms. Its therapeutic use is mainly limited by nephrotoxicity. This study was aimed at evaluating the effect of rutin on oxidative stress, inflammation, apoptosis, and autophagy in gentamicin-induced nephrotoxicity in rats. The rats were treated with saline intraperitoneally (group I), 150 mg/kg of rutin orally (group II), 80 mg/kg of gentamicin intraperitoneally for 8 d (group III), or 150 mg/kg of rutin plus 80 mg/kg of gentamicin (group IV). The serum urea, creatinine, kidney malondialdehyde (MDA), and reduced glutathione (GSH) levels and superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) activity and protein concentration were measured, and renal histopathology analysis and immunohistochemical staining were performed. Rutin pretreatment attenuated nephrotoxicity induced by gentamicin by reducing the urea, creatinine, and MDA levels and increasing the SOD, CAT, and GPx activity, and the GSH levels. The rutin also inhibited inducible nitric oxide synthase (iNOS), cleaved caspase-3 and light chain 3B (LC3B), as evidenced by immunohistochemical staining. The present study demonstrates that rutin exhibits antioxidant, anti-inflammatory, anti-apoptotic, and anti-autophagic effects and that it attenuates gentamicin-induced nephrotoxicity in rats.