Mustafa Erboga

Role of quercetin in cadmium-induced oxidative stress, neuronal damage, and apoptosis in rats:

The present study was carried out to evaluate the neuroprotective effect of quercetin (QE) in protecting the cadmium (Cd)-induced neuronal injury in frontal cortex of rats. A total of 30 adult male Sprague-Dawley rats were randomly divided into three groups of 10 animals each: control, Cd treated and Cd treated with QE. The Cd-treated group was injected subcutaneously with cadmium chloride (CdCl2) dissolved in saline at a dose of 2 ml/kg/day for 30 days, resulting in a dosage of 1 mg/kg Cd. The rats in QE-treated groups were given QE (15 mg/kg body weight) once a day intraperitoneally starting 2 days prior to Cd injection, during the study period. Rats were sacrificed at the end of the study and the frontal cortex tissues were removed for biochemical and histopathological investigation. To date, there is no available information on the effect of QE on neuronal injury after Cd exposure. Rats intoxicated with Cd for 30 days, significantly increased tissue malondialdehyde (MDA) levels and significantly decreased enzymatic antioxidants superoxide dismutase, glutathione peroxidase and catalase in the frontal cortex tissue. Administration of QE with Cd significantly diminished the levels of MDA and significantly elevated the levels of enzymatic antioxidants in the frontal cortex tissue. The histopathological studies in the brain of rats also supported that QE markedly reduced the Cd-induced histopathological changes and well preserved the normal histological architecture of the frontal cortex tissue. The caspase-3 immunopositivity was increased in degenerating neurons of the Cd group. Treatment with QE markedly reduced the immunoreactivity of degenerating neurons. In conclusion, the results of the current study suggest that QE may be beneficial in combating the Cd-induced neurotoxicity in the brain of rats. We believe that further preclinical research into the utility of QE may indicate its usefulness as a potential treatment for neurodegeneration after Cd exposure in rats.

Protective effects of fish omega‐3 fatty acids on doxorubicin‐induced testicular apoptosis and oxidative damage in rats

The aim of this study was to examine the protective effects of fish omega‐3 (n‐3) fatty acids on acute doxorubicin (DOX)‐induced testicular apoptosis and oxidative damage. 24 male rats were divided into three groups: control, DOX‐treated and DOX+fish n‐3 fatty acids. Fish n‐3 fatty acids (400 mg kg−1) were given for 30 days by intragastric gavage. The rats received a single intraperitoneal injection of DOX (30 mg kg−1) and were sacrificed after 48 h. The DOX+fish n‐3 fatty acids group showed a decrease in malondialdehyde levels and increased activities of superoxide dismutase and glutathione peroxidase in comparison with the DOX‐treated group. Acute DOX treatment caused severe damage such as disorganisation and separation of germ cells. The fish n‐3 fatty acids‐pretreated rats showed an improved histological appearance in the DOX‐treated group. Our data indicate a reduction in the activity of terminal deoxynucleotidyl transferase mediated dUTP nick end labelling; there was a rise in the expression of proliferating cell nuclear antigen in testis tissues of the DOX+fish n‐3 fatty acids group compared with DOX‐treated group. These data suggested that fish n‐3 fatty acids pre‐treatment may be beneficial for spermatogenesis following acute DOX‐induced testicular damage by decreasing germ cell apoptosis and oxidative stress.

Neuroprotective effect of quercetin against oxidative damage and neuronal apoptosis caused by cadmium in hippocampus

The purpose of the present investigation was to evaluate cadmium (Cd)-induced neurotoxicity in hippocampal tissues and beneficial effect of quercetin (QE) against neuronal damage. A total of 30 male rats were divided into 3 groups: control, Cd-treated, and Cd + QE-treated groups. After the treatment, the animals were killed and hippocampal tissues were removed for biochemical and histopathological investigation. Cd significantly increased tissue malondialdehyde (MDA) and protein carbonyl (PC) levels and also decreased superoxide dismutase (SOD) and catalase (CAT) enzyme activities in hippocampal tissue compared with the control. Administration of QE with Cd significantly decreased the levels of MDA and PC and significantly elevated the levels of antioxidant enzymes in hippocampal tissue. In the Cd-treated group, the neurons of both tissues became extensively dark and degenerated with pyknotic nuclei. The morphology of neurons in Cd + QE group was well protected, but not as neurons of the control group. The caspase-3 immunopositivity was increased in degenerating neurons of the Cd-treated group. Treatment of QE markedly reduced the immunoreactivity of degenerating neurons. The results of the present study show that QE therapy causes morphologic improvement in neurodegeneration of hippocampus after Cd exposure in rats.

Protective effects of thymoquinone against apoptosis and oxidative stress by arsenic in rat kidney

Abstract We aimed to investigate the protective role of thymoquinone (TQ) by targeting its antiapoptotic and antioxidant properties against kidney damage induced by arsenic in rats. We have used the 24 male Sprague-Dawley rats. Rats were divided into three groups. Physiological serum in 10 mL/kg dose as intragastric was given to the control group. Sodium arsenite (10 mg/kg, intragastric by gavage for fifteen days) was given to the arsenic group. Sodium arsenite (10 mg/kg, intragastric by gavage for fifteen days) and TQ (10 mg/kg, intragastric by gavage for 15 days) was given to the arsenic + TQ group. After 15 days, the animals’ kidneys were taken theirs, then we have performed histological and apoptotic assessment. Superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) enzyme activities and malondialdehyde (MDA) levels have examined as the oxidative stress parameters. We have determined the levels of arsenic. Increased renal injury and apoptotic cells have been detected in the arsenic group. Degenerative changes in the arsenic + TQ group were diminished. Although the MDA levels were augmented in the arsenic group, SOD, CAT and GSH-Px enzyme activities were lessened than the other groups. Our findings suggest that TQ may impede the oxidative stress, the cells have been damaged and also the generation of apoptotic cells arisen from arsenic. TQ plays a protective role against arsenic-induced toxicity in kidney and may potentially be used as a remedial agent.

Effects of Urtica dioica on oxidative stress, proliferation and apoptosis after partial hepatectomy in rats

The present study was performed to investigate the effect of Urtica dioica (UD) on liver regeneration after partial hepatectomy (PH) in rats. A total of 24 male Sprague Dawley rats were divided into three groups: sham-operated, PH and PH + UD; each group contains eight animals. The rats in UD-treated groups were given UD oils (2 ml/kg/day) once a day orally for 7 days starting 3 days prior to hepatectomy operation. At day 7 after resection, liver samples were collected. The levels of malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione (GSH) were estimated in liver homogenates. Moreover, histopathological examination, mitotic index (MI), proliferating cell nuclear antigen labeling, proliferation index (PI), transferase-mediated deoxyuridine triphosphate nick end-labeling assay, apoptotic index (AI) were evaluated at day 7 after hepatectomy. As a result, UD significantly increased MI and PI, significantly decreased AI and also attenuated hepatic vacuolar degeneration and sinusoidal congestion in PH rats. UD treatment significantly decreased the elevated tissue MDA level and increased the reduced SOD activity and GSH level in the tissues. These results suggest that UD pretreatment was beneficial for rat liver regeneration after partial hepatectomy.

Neuroprotective effect of ebselen against intracerebroventricular streptozotocin-induced neuronal apoptosis and oxidative stress in rats

The goal of this study was to examine the neuroprotective effect of ebselen against intracerebroventricular streptozotocin (ICV-STZ)-induced oxidative stress and neuronal apoptosis in rat brain. A total of 30 adult male Sprague-Dawley rats were randomly divided into 3 groups of 10 animals each: control, ICV-STZ, and ICV-STZ treated with ebselen. The ICV-STZ group rats were injected bilaterally with ICV-STZ (3 mg/kg) on days 1 and 3, and ebselen (10 mg/kg/day) was administered for 14 days starting from 1st day of ICV-STZ injection to day 14. Rats were killed at the end of the study and brain tissues were removed for biochemical and histopathological investigation. Our results demonstrated, for the first time, the neuroprotective effect of ebselen on Alzheimer’s disease (AD) model in rats. Our present study, in ICV-STZ group, showed significant increase in tissue malondialdehyde levels and significant decrease in enzymatic antioxidants superoxide dismutase and glutathione peroxidase in the frontal cortex tissue. The histopathological studies in the brain of rats also supported that ebselen markedly reduced the ICV-STZ-induced histopathological changes and well preserved the normal histological architecture of the frontal cortex tissue. The number of apoptotic neurons was increased in frontal cortex tissue after ICV-STZ administration. Treatment of ebselen markedly reduced the number of degenerating apoptotic neurons. The study demonstrates the effectiveness of ebselen, as a powerful antioxidant, in preventing the oxidative damage and morphological changes caused by ICV-STZ in rats. Thus, ebselen may have a therapeutic value for the treatment of AD.

The Effects of Ferulic Acid Against Oxidative Stress and Inflammation in Formaldehyde-Induced Hepatotoxicity

This study was designed to elucidate the protective effects of ferulic acid (FA) on formaldehyde-induced hepatotoxicity by measuring some routine biochemical parameters, cytokine levels, and oxidative stress-related parameters in addition to YKL-40 in male Wistar albino rats. Tissue superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) activities, and tissue malondialdehyde (MDA) levels were measured. Also, serum YKL-40, TNF-α, IL-6, IL-1β, IL-8, total protein, albumin, total bilirubin concentrations, and AST, ALT, ALP, and LDH activities were measured. Histological specimens were examined in light microscopy. Formaldehyde significantly increased tissue MDA, and serum cytokine levels and also decreased activities of antioxidant enzymes. FA treatment decreased MDA and cytokine levels and increased activities of antioxidant enzymes. FA also alleviated degeneration due to formaldehyde toxicity. We suggested that FA can be used as a promising hepatoprotective agent against formaldehyde toxicity because of the obvious beneficial effects on oxidative stress parameters.

Antioxidative, antiapoptotic, and proliferative effect of curcumin on liver regeneration after partial hepatectomy in rats

The aim of the present study was to assess the influence of curcumin on liver regeneration after partial hepatectomy (PH) in rats. A total of 24 male Sprague Dawley rats were divided into three groups: sham-operated (SH), PH, and PH + curcumin; each group contains eight animals. The rats in curcumin-treated groups were given curcumin (in a dose of 100 mg/kg body weight) once a day orally for 7 days, starting 3 days prior to hepatectomy operation. At 7 days after resection, liver samples were collected. The malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione (GSH) levels were estimated in liver homogenates. Moreover, histopathological examination, mitotic index (MI), proliferating cell nuclear antigen labeling, proliferation index (PI), transferase-mediated 2′-deoxyuridine, 5′-triphosphate nick end-labeling assay, and apoptotic index (AI) were evaluated at 7 days after hepatectomy. As a result, curcumin significantly increased MI and PI and significantly decreased AI in PH rats. Additionally, curcumin remarkably inhibited MDA elevation, restored impaired antioxidant SOD activity and GSH level and also attenuated hepatic vacuolar degeneration and sinusoidal congestion. These results suggested that curcumin treatment had a beneficial effect on liver regenerative capacity of the remnant liver tissue after hepatectomy, probably due to its antioxidative, antiapoptotic, and proliferative properties.

Protective effects of thymoquinone on experimental testicular ischaemia–reperfusion injury: an apoptotic, proliferative and biochemical study

The objective of this study was to examine the effects of thymoquinone (TQ), which has antioxidant properties in the experimental testicular I/R model in rats in terms of its anti‐apoptotic, proliferative and biochemical attributes. In our study, 24 male rats were divided into three groups: control group, I/R group and I/R+TQ group. Testicular torsion was created by rotating the left testis 720° in a clockwise direction. The ischaemia period was 4 h, and an orchiectomy was performed after 4 h of detorsion. Spermatogenesis and the mean seminiferous tubule diameter were significantly decreased in the I/R groups compared to the control group. Furthermore, TQ‐treated animals displayed an improved histological appearance in the I/R group. It was also observed that treatment with TQ increased the activity of PCNA, which decreased as a result of I/R, and this treatment also reduced the number of TUNEL‐positive cells. The I/R+TQ group showed a decrease in malondialdehyde levels and an increase in the activities of superoxide dismutase, catalase and glutathione peroxidase in comparison with the I/R group. It could be concluded that cytoprotective effects of TQ on the I/R testicles are via reduction of apoptosis, oxidative stress and lipid peroxidation.

Protective effects of Nigella sativa on gamma radiation-induced jejunal mucosal damage in rats.

INTRODUCTION The aim of this study was to compare the efficacy of Nigella sativa in protection of jejunal mucosa against harmful effects of gamma radiation. METHODS Radiotherapy group received abdominal gamma radiation of 15Gy in addition to physiological saline. Radiotherapy+Nigella sativa treatment group received abdominal gamma radiation of 15Gy in addition to Nigella sativa treatment in the amount of 400mg/kg. Radiotherapy and treatment groups were sacrificed 3 days after the exposure to irradiation. Then, jejunum samples were harvested for biochemical and histological assessment of mucosal injury. RESULTS Nigella sativa treatment was found to significantly lower elevated tissue malondialdehyde (MDA) levels and, to raise reduced glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) activity in intestinal tissues samples. Single dose 15Gy gamma-irradiation was noted to result in a marked jejunal mucosal injury. Three days after exposure to irradiation, the villi and Lieberkühn crypts were observed as denuded, and villous height diminished. Concomitantly with inflammatory cell invasion, capillary congestion and ulceration were observed in the atrophic mucosa. Nigella sativa treatment significantly attenuated the radiation induced morphological changes in the irradiated rat jejunal mucosa. CONCLUSION Nigella sativa has protective effects against radiation-induced damage, suggesting that clinical transfer is feasible.