Elçin Hakan Terzi

Interleukin 10 reduces testicular damage in experimental testicular ischemia/reperfusion injury.

OBJECTIVE To evaluate the protective effect of interleukin 10 (IL-10) on biochemical and histopathologic changes in experimental testicular ischemia or reperfusion injury (RI) in rats. METHODS Sprague-Dawley rats were randomly divided into 3 groups, each containing 7 rats; sham-control, I-R/untreated group, and I/R treated with IL-10. The ischemia period was 6 hours, and orchiectomy was performed after 1 hour of detorsion. IL-10 was given intraperitoneally in a period of 10 minutes before reperfusion. In all groups, ipsilateral orchiectomies were performed to make histologic examination and biochemical analysis such as malondialdehyde, glutathione peroxidase, and myeloperoxidase (MPO). RESULTS IL-10 treatment significantly decreased the I-R-induced elevation in testes malondialdehyde levels. In the I-R/IL-10-treated group, testes glutathione peroxidase levels were increased compared with the I-R/untreated group rats. MPO activities were significantly increased in the testes tissues of the I-R/untreated group. However, in the I-R/IL-10-treated group, MPO levels significantly decreased. Histopathologically, in the I-R/untreated group rats, edema, congestion, hemorrhage among seminiferous tubules, and necrosis of the germinal cells were predominant features in sections. The testicular injury score was lower in the IL-10-treated group rats compared with the I-R/untreated group. CONCLUSION IL-10 might play a protective role in reducing reperfusion injury.

Protective effect of montelukast, a cysteinyl leukotriene receptor-1 antagonist, against intestinal ischemia-reperfusion injury in the rat.

Abstract Objective : Ischemia-reperfusion (I-R) injury of the intestine is a significant problem because the initial damage caused by ischemia is exacerbated by reperfusion. In this study, we examined the protective effect of montelukast against I-R-induced intestinal tissue damage. Materials and methods : Eight-week-old male Sprague-Dawley rats were randomly divided into three treatment groups: a sham-operated group, a group receiving I-R, and a group receiving I-R plus montelukast (I-R/M). Tissue samples were evaluated and scored histologically. The blood levels of malondialdehyde (MDA), myeloperoxidase (MPO), glutathione (GSH), and cardiotrophin-1 (CT-1) were measured. Results : In the I-R group, the histological score and the levels of serum MDA and MPO were increased compared with those in the control group. In the I-R/M group, the histological score and serum MDA and MPO levels were significantly decreased compared with those in the I-R group. Additionally, compared with the IR group, the I-R/M group had increased serum GSH and CT-1 levels and a decreased intestinal injury score. Ileal sections from the I-R/M group showed minimal alterations, characterized by moderate lifting of the epithelial layer from the lamina propria, and few apoptotic enterocytes were observed compare with the number in the I-R group. Conclusion : The findings of the present study demonstrated that montelukast can protect I-R-induced intestinal damage in rats.

Methylene blue attenuates renal ischemia–reperfusion injury in rats

BACKGROUND AND PURPOSE In our study, we investigated the effects of methylene blue (MB) on histopathological changes in renal ischemia/reperfusion (I/R) injury rat model. MATERIAL AND METHODS Twenty-one Sprague-Dawley male rats were divided equally into three groups. Group 1 (control) was administered intraperitoneal saline solution. In Groups 2 (untreated group) and 3 (MB treatment), the renal arteries were clamped, and ischemia (for 1 hour) and then reperfusion (for 4 hours) were applied. Thirty minutes before ischemia, the untreated group received physiological saline, whereas the treatment group was administered 30 mg/kg MB through an intraperitoneal route. Blood samples were drawn, and renal specimens were harvested 5.5 hours after physiologic saline injection in the control and immediately after the reperfusion period in the other groups. The levels of tissue superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), total oxidant status (TOS), total antioxidant status (TAS), plasma urea, creatinine and ischemia modified albumin (IMA) were measured. Moreover, the histopathological damage score of the renal tissue was determined. RESULTS MB significantly alleviated the severity of histopathological damage by increasing the levels of tissue SOD and TAS and decreasing TOS concentrations in the renal I/R model (p<0.05). CONCLUSION Administration of MB in renal I/R damage may play a protective role.

Comparison of Histopathological Effects of Thymoquinone and Local Nasal Corticosteroids in Allergic Rhinitis in a Rabbit Model.

Background/Aims: In this study, we aimed to evaluate the histopathological effects of thymoquinone treatment of the nasal mucosa in a rabbit model of allergic rhinitis, and we compared its effects with those of nasal mometasone furoate. Methods: A total of 24 male New Zealand rabbits were used. The animals were randomly assigned to one of four groups. Group 1 received no treatment, while group 2 underwent ovalbumin (OVA) sensitization only. Group 3 was the study group; after OVA sensitization, the rabbits were treated with intranasal thymoquinone. The group 4 rabbits received mometasone furoate for 7 days after OVA sensitization. Mucosal structures were stained with hematoxylin and eosin, while toluidine blue was used to stain mast cells. Apoptosis was evaluated using a TUNEL assay. Results: In the positive control groups, including the thymoquinone and intranasal mometasone furoate groups, intraepithelial and submucosal inflammation and goblet cell hypertrophy were significantly decreased compared to group 2 (p < 0.001). The cilial structure was normal, as was the chondrocyte structure in both treatment groups. Conclusion: This is the first study to evaluate the histopathological effects of thymoquinone in an allergic rhinitis model. Thymoquinone reduced allergic inflammation and may be valuable for treating allergic rhinitis. However, additional studies are needed.

The histopathological and electrophysiological effects of thymoquinone and methylprednisolone in a rabbit traumatic facial nerve paralysis model

OBJECTIVE We aimed to determine the effects of methylprednisolone and thymoquinone on nerve healing in a traumatic facial nerve paralysis animal model. SUBJECTS AND METHODS Twenty-four rabbits were randomly divided into 4 groups: group I: control group received no medication and no trauma; group II: sham group received no medication after facial nerve trauma group III: 5mg/kg/day thymoquinone administered; group IV: 1mg/kg/day methylprednisolone administered. An initial electrophysiological assessment was performed in all the animals. The buccal branch of the facial nerve was then clipped to form a traumatic facial paralysis model. The drugs were administered for two weeks once a day. At the end of the second month, the electrophysiological assessments were performed and the distal part of the traumatic facial nerve were dissected and examined under light microscopy. RESULTS Best nerve regeneration was observed in the control and the thymoquinone groups, respectively, whereas the weakest regeneration was determined in the sham group. Thymoquinone and methylprednisolone significantly increased nerve recovery, as measured by histopathological scores and electrophysiological assessment. In the thymoquinone group, due to postoperative amplitude, axon diameter and thickness of myelin sheath values were significantly further increased nerve regeneration compared to that of the methylprednisolone group and these values were close to those of the values of the control group. CONCLUSION Thymoquinone was slightly better than methylprednisolone for functional nerve recovery. The neuroprotective effect of thymoquinone was attributed to its antioxidant and anti-inflammatory effects. Thymoquinone can have a new treatment option to ameliorate the nerve injury.

Histopathological evaluation of the effect of intranasal phototherapy on nasal mucosa in rabbits

Allergic rhinitis is a high-incidence allergic inflammation of the nasal airways that impacts quality of life. Of the numerous therapies used to treat allergic rhinitis, intranasal phototherapy has emerged as a promising new treatment modality for inflammatory airway disease. Phototherapy is widely used for the treatment of immune-mediated skin diseases because its profound immunosuppressive effect inhibits hypersensitivity reactions in the skin. Intranasal phototherapy using a combination of Ultraviolet-A (UVA) and Ultraviolet-B (UVB) plus Visible light (VIS) has been shown to suppress the clinical symptoms of allergic rhinitis, but limited data regarding its adverse effects on the nasal mucosa currently exists. In this study, we demonstrate that UV displays no harmful effects on the nasal mucosa cells of rabbits following 2 weeks of intranasal phototherapy.

Histopathological effects of intranasal phototherapy and nasal corticosteroids in allergic rhinitis in a rabbit model

Allergic rhinitis is one of the most common health problems and has a major effect on quality of life. Although new-generation antihistamines and nasal steroids are the main treatment options, complete resolution cannot be obtained in some patients. Besides common side effects such as nasal irritation and epistaxis, the use of these drugs is controversial in some patients, such as pregnant or breastfeeding women. These findings highlight the need for new treatment options. Although phototherapy has been successfully used in the treatment of atopic dermatitis, which is an IgE-mediated disease and shares several common pathogenic features with allergic rhinitis, there are limited studies about its role in the treatment of allergic rhinitis. In this study, we aimed to evaluate and compare the histopathological effects of intranasal phototherapy (Rhinolight) and nasal corticosteroid treatment on the nasal mucosa in allergic rhinitis in a rabbit model and we found that both treatment options significantly reduced inflammation in the nasal mucosa without increasing apoptosis of mucosal cells.