The effect of magnetic field therapy and electric stimulation on experimental burn healing.

OBJECTIVES: : In this study, we aimed to compare morphological and histological differences between magnetic field and electric stimulation therapies in an experimental burn injury model in rats. MATERIALS AND METHODS: Between February 2011 and July 2011, a total of 21 Sprague-Dawley female rats were used in this study. Second-degree burns were induced on the back areas of the rats. All rats were equally divided into three groups including seven in each: the first burn group was treated with antibacterial pomade (Group 1, control group); the second group was treated with both antibacterial pomade and pulsed electromagnetic field therapy (Group 2); and the third group was treated with antibacterial pomade and electric stimulation for 14 days (Group 3). RESULTS: Earlier re-epithelialization, wound area contraction, reduction of edema, and hyperaemia were observed on gross examination in the pulsed electromagnetic fields and electric stimulation therapy groups compared to the control group. Neovascularization, collagen density, granulation tissue formation, cell proliferation, and inflammatory cell response of the pulsed electromagnetic fields and electric stimulation group increased, compared to the control group, in the histopathological evaluation (p<0.05). CONCLUSION: Our study results showed the positive healing effects of electric stimulation and pulsed electromagnetic fields on burn injury. Pulsed electromagnetic fields therapy produced more positive signs of healing than the electric stimulation group.

Effect of Mitomycin - C and Triamcinolone on Preventing Urethral Strictures

ABSTRACT Urethral stricture is a common disease with high recurrence rate. Several manipulations were defined to prevent the recurrence but the results were disappointing. This study aimed to evaluate the efficacy of triamcinolone and mitomycin-C on urethral stricture formation and their effect on inhibition of urethral fibrosis. A total of 24 New Zealand rabbits were divided into 3 groups. Urethras of rabbits were traumatized with pediatric resectoscope. Resection area was irrigated with 10mL saline, swapped with a cotton wool soaked with 0.5mg/mL MMC and injected by 40mg triamcinolone in groups 1, 2 and 3 respectively. Retrograde urethrogram was performed at 28th day of procedure and the urethra was removed for histopathologic evaluation. There were significant differences in urethral diameters and in lumen reduction rate between the control and study groups (p<0.001). Compared to control group, all treatment groups showed mild fibrosis, less collagen bundle irregularity, and lower numbers of fibroblasts (p=0.003). The Tunnel assay showed that the number of apoptotic cells in the submucosal connective tissue was quantitatively higher in control groups (p=0.034). In the view of efficacy and safety, MMC and triamcinolone have the potential to replace the use of stents, clean intermittent catheterization, or long term catheters following internal urethrotomy. There were no statistically significant differences between two agents in terms of preventing urethral stricture formation in the present study. Mitomycin C and triamcinolone decreased the recurrence rates of urethral stricture.

Effect of Mitomycin - C and Triamcinolone on Preventing Urethral Strictures.

Urethral stricture is a common disease with high recurrence rate. Several manipulations were defined to prevent the recurrence but the results were disappointing. This study aimed to evaluate the efficacy of triamcinolone and mitomycin-C on urethral stricture formation and their effect on inhibition of urethral fibrosis. A total of 24 New Zealand rabbits were divided into 3 groups. Urethras of rabbits were traumatized with pediatric resectoscope. Resection area was irrigated with 10mL saline, swapped with a cotton wool soaked with 0.5mg/mL MMC and injected by 40mg triamcinolone in groups 1, 2 and 3 respectively. Retrograde urethrogram was performed at 28th day of procedure and the urethra was removed for histopathologic evaluation. There were significant differences in urethral diameters and in lumen reduction rate between the control and study groups (p<0.001). Compared to control group, all treatment groups showed mild fibrosis, less collagen bundle irregularity, and lower numbers of fibroblasts (p=0.003). The Tunnel assay showed that the number of apoptotic cells in the submucosal connective tissue was quantitatively higher in control groups (p=0.034). In the view of efficacy and safety, MMC and triamcinolone have the potential to replace the use of stents, clean intermittent catheterization, or long term catheters following internal urethrotomy. There were no statistically significant differences between two agents in terms of preventing urethral stricture formation in the present study. Mitomycin C and triamcinolone decreased the recurrence rates of urethral stricture.

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-1ß, 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.

Protective Effect of Nigella Sativa on Renal Reperfusion Injury in Rat.

INTRODUCTION: This study was designed to investigate the effect of Nigella sativa (NS), in reperfusion-induced renal injury in rats. MATERIALS AND METHODS: A total of 24 male Sprague-Dawley rats were divided into 3 groups of controls and rats that underwent ischemia-reperfusion with and without pretreatment with NS. A rat model of renal reperfusion injury was induced by 45-minute occlusion of the bilateral renal pedicles and 24-hour reperfusion. In the NS group, a single dose NS (400 mg/kg orally) was administered by gastric gavage. RESULTS: Renal reperfusion caused severe histopathological injury such as tubular damage, atrophy dilatation, loss of brush border, and hydropic epithelial cell degenerations. Treatment with NS significantly attenuated the severity of reperfusion injury and significantly lowered tubulointerstitial damage score as compared with the reperfusion group. When kidney sections were stained with anti-proliferating-cell nuclear antigen antibody, nuclear factor kappaB p65 antibody, and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling, there was a clear increase in the number of positive cells in the reperfusion group in the renal cortical tissues. However, there was a significant reduction in the number of stain-positive cells in kidney tissue from the NS group. Treatment of renal reperfusion injury with NS decreased the elevated tissue malondialdehyde levels and increased the reduced activities of the enzymatic antioxidants glutathione peroxidase and catalase. CONCLUSIONS: Pretreatment with NS has a protective effect against renal damage induced by renal reperfusion. This protective effect is possibly due to its ability to inhibit reperfusion-induced renal damage, apoptosis, and cell proliferation.

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.

Mannitol has a protective effect on testicular torsion: An experimental rat model.

OBJECTIVE: Testicular torsion is an emergency condition that causes testicular injury. Any treatment opportunity reducing the destructive effect of testicular torsion is important for the future life of patients. In this experimental study we investigated the protective effect of mannitol on ischemia-reperfusion (I/R) injury in a rat testes torsion model. METHOD: In total, 32 male Sprague Dawley rats were included. Four experimental groups included eight rats each. Group A was a sham group in which the right testis was brought out through a scrotal incision and then replaced in the scrotum without torsion. In Group B, the right testis was torsioned, by rotating 720° clockwise and fixed to the scrotum with no treatment. In Group C, the same testicular torsion process was performed with saline infusion just after testicular torsion. In group D, mannitol infusion was used just after testicular torsion. Testicles were detorsioned after 3 h and left inside for more than 2 h before orchiectomy. Histopathological, immunohistochemical, and biochemical analyses were performed. RESULTS: Testicular architecture was disturbed significantly in the torsion groups without mannitol infusion. However, testicular tissue structure was significantly better in the mannitol-treated group, demonstrating a protective effect. Similar findings were also shown for the proliferating cell nuclear antigen (PCNA) index and antioxidant activity; both were higher in the mannitol group than in the no-treatment and saline groups (p < 0.01). The apoptotic index was also significantly lower in the mannitol-treated group compared with the no treatment and saline groups (p < 0.01). CONCLUSIONS: The seminiferous tubule structure in testicular torsion without mannitol treatment was significantly disturbed, whereas the structural disruption was considerably less in the mannitol group. Mannitol treatment also decreased reactive oxygen radical levels significantly and was able to decrease apoptosis. These results were consistent with other organ model studies that evaluated the protective effects of mannitol treatment in I/R injury. Mannitol infusion had a protective effect against I/R injury in testicular torsion in rats. This experimental study may guide clinicians to evaluate the effectiveness of mannitol in human testicular torsion.

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

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.

Protective Effect of Infliximab, a Tumor Necrosis Factor-Alfa Inhibitor, on Bleomycin-Induced Lung Fibrosis in Rats.

We aimed to investigate the preventive effect of Infliximab (IFX), a tumor necrosis factor (TNF)-α inhibitor, on bleomycin (BLC)-induced lung fibrosis in rats. Rats were assigned into four groups as follows: I-BLC group, a single intra-tracheal BLC (2.5 mg/kg) was installed; II-control group, a single intra-tracheal saline was installed; III-IFX + BLC group, a single-dose IFX (7 mg/kg) was administered intraperitoneally (i.p.), 72 h before the intra-tracheal BLC installation; IV-IFX group, IFX (7 mg/kg) was administered alone i.p. on the same day with IFX + BLC group. All animals were sacrificed on the 14th day of BLC installation. Levels of tumor necrosis factor (TNF)-α, transforming growth factor (TGF)-ß, interleukin (IL)-6, periostin, YKL-40, nitric oxide (NO) in rat serum were measured, as well as, myeloperoxidase (MPO), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) activity, and reduced glutathione (GSH), hydroxyproline, malondialdehyde (MDA) content in lung homogenates. Lung tissues were stained with hematoxylin and eosin (H&E) for quantitative histological evaluation. The inducible nitric oxide synthase (iNOS) expression and cell apoptosis in the lung tissues were determined quantitatively by immunohistochemical staining (INOS) and by TUNNEL staining, respectively. BLC installation worsened antioxidant status (such as SOD, CAT, GPx, GSH, MPO), while it increased the serum TNF-α, TGF-ß, IL-6, periostin, YKL-40, and lipid peroxidation, and collagen deposition, measured by MDA and hydroxyproline, respectively. IFX pretreatment improved antioxidant status as well as BLC-induced lung pathological changes, while it decreased the TNF-α, TGF-ß, IL-6, periostin, YKL-40, lipid peroxidation and collagen deposition. Finally, histological, immunohistochemical, and TUNNEL evidence also supported the ability of IFX to prevent BLC-induced lung fibrosis. The results of the present study indicate that IFX pretreatment can attenuate BLC-induced pulmonary fibrosis.

Anti-Apoptotic and Anti-Oxidant Effects of Caffeic Acid Phenethyl Ester on Cadmium-Induced Testicular Toxicity in Rats.

Cadmium (Cd) is a serious environmental and occupational contaminant and may represent a serious health hazard to humans and other animals. Cd is reported to induce the generation of reactive oxygen species, and induces testicular damage in many species of animals. The goal of our study was to examine the anti-apoptotic and anti-oxidant effects of caffeic acid phenethyl ester (CAPE) on Cd-induced oxidative stress, apoptosis, and testicular injury in rats. A total of 40 male Wistar albino rats were divided into four groups: control, CAPE alone, Cd-treated, and Cd-treated with CAPE; each group consisted of 10 animals. To induce toxicity, Cd (1 mg/kg body weight) was dissolved in normal saline and subcutaneously injected into rats for 30 days. The rats in CAPE-treated group were given a daily dose of 10 µmol/kg body weight of CAPE by using intraperitoneal injection. This application was continued daily for a total of 30 days. To date, no examinations of the anti-apoptotic and anti-oxidant properties of CAPE on Cd-induced apoptosis, oxidative damage, and testicular injury in rat testes have been reported. CAPE-treated animals showed an improved histological appearance and serum testosterone levels in Cd-treated group. Our data indicate a significant reduction in the number of apoptotic cells in testis tissues of the Cd-treated group with CAPE treatment. Moreover, CAPE significantly suppressed lipid peroxidation, compensated deficits in the anti-oxidant defenses in testes tissue resulted from Cd administration. These findings suggest that the protective potential of CAPE in Cd toxicity might be due to its anti-oxidant and anti-apoptotic properties, which could be useful for achieving optimum effects in Cd-induced testicular injury.

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.

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.

Effect of Cadmium on Trophoblast Cell Proliferation and Apoptosis in Different Gestation Periods of Rat Placenta.

In this study, we aimed to show how cadmium (Cd) affects the trophoblast proliferation and differentiation in the placenta and the apoptotic activity in different gestational days and, hence, its effects of placental development with immunohistochemical and TUNEL techniques. Experimental model of our study consisted of placental development of control and Cd groups on 15, 17, 19, and 21th days of the gestation. Female rats in Cd groups were subcutaneously administered a single dose of 0.5 mg Cd/kg/day dissolved in sodium chloride as 2 mL/kg Cd chloride until the day they sacrificed. Embryo and placenta of female rats were separately removed on 15, 17, 19, and 21th days of the gestation in which the placental development takes place and placentas were processed for microscopic examinations. In the placentas of the control group, all layers were observed to be formed on the 15th gestational day and thereafter a continuous growth was monitored. In the Cd group also all layers existed from the 15th gestational day. However, they were smaller in size than control groups. Frequency of proliferating cell nuclear antigen (PCNA)-positive cells was decreased and the number of apoptotic cells was increased in all the gestational days related to Cd. In conclusion, Cd administered during the pregnancy was observed to cause abnormal placental development by disrupting the normal structure of the placenta, inhibiting the proliferation of trophoblast and increasing the number of apoptotic trophoblast cells.

Thymoquinone Ameliorates Cadmium-Induced Nephrotoxicity, Apoptosis, and Oxidative Stress in Rats is Based on its Anti-Apoptotic and Anti-Oxidant Properties.

Cadmium (Cd), an environmental and industrial pollutant, generates free radicals responsible for oxidative stress. Cd can also lead to various renal toxic damage such as the proximal tubules and glomerulus dysfunction. Thymoquinone (TQ) is the main constituent of the essential oil obtained from black seeds (Nigella sativa) and has various pharmacological effects. The aim of the present study was to examine the nephroprotective, anti-oxidant, and anti-apoptotic effect of the TQ against Cd-induced nephrotoxicity. A total of 24 male Wistar albino rats were divided into three groups: control, Cd-treated, and Cd-treated with TQ; each group contain eight animals. The Cd-treated group was injected subcutaneously with CdCl2 dissolved in saline in the amount of 2 ml/kg/day for 30 days, resulting in a dosage of 1 mg/kg Cd. The rats in TQ-treated groups were given TQ (50 mg/kg body weight) once a day orally together with first Cd injection during the study period. The histopathological studies in the kidney of rats also showed that TQ markedly reduced the toxicity of Cd and preserved the normal histological architecture of the renal tissue. Immunohistochemical analysis revealed that TQ significantly decreased the Cd-induced over expression of nuclear factor-κB in renal tissue. Furthermore, TQ treatment resulted in decreased the number of apoptotic cells. TQ significantly suppressed lipid peroxidation, compensated deficits in the anti-oxidant defenses (reduced superoxide dismutase, glutathione peroxidase and catalase activities) in renal tissue resulted from Cd administration. These findings suggest that the nephroprotective potential of TQ in Cd toxicity might be due to its anti-oxidant and anti-apoptotic properties, which could be useful for achieving optimum effects in Cd-induced nephrotoxicity.

Quercetin ameliorates methotrexate-induced renal damage, apoptosis and oxidative stress in rats.

BACKGROUND: In the present study, the protective and therapeutic effects of quercetin (QE) on renal injury induced by methotrexate (MTX) have been examined. MATERIALS AND METHODS: A total of 24 male rats were divided into the following three groups: control group, MTX group, and MTX + QE group. Rats in MTX group received 20 mg/kg of single dose of MTX, while those in MTX + QE group received 20 mg/kg of single dose MTX, in addition to 15 mg/kg of QE administered 30 min prior to MTX and in the following 5-day period as a single daily dose. At the end of the experimental period, renal tissues were removed for histopathological and biochemical assessments. RESULTS: Light microscopic examination showed a disruption of the renal structure in rats in MTX group in the form of tubular degeneration and dilation, with shedding of the tubular epithelial cells into the lumen. QE treatment was associated with less marked degenerative changes, with a similar histological appearance to that of controls. Furthermore, QE treatment resulted in decreased the number of apoptotic cells. Biochemical assessments showed significantly higher malondialdehyde (MDA) levels in MTX group as compared to control and MTX + QE groups. superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT) levels showed a significant decrease in MTX group as compared to controls. However, QE significantly suppressed MDA level, compensated deficits in the anti-oxidant defenses [reduced SOD, GSH-Px, and CAT levels] in kidney tissue resulted from MTX administration. CONCLUSIONS: In conclusion, renal toxic effects of MTX may be alleviated by QE.

The effect of methylene blue treatment on aspiration pneumonia.

BACKGROUND: The study aimed to examine whether methylene blue (MB) prevents different pulmonary aspiration materials-induced lung injury in rats. METHODS: The experiments were designed in 60 Sprague-Dawley rats, ranging in weight from 250-300 g, randomly allotted into one of six groups (n = 10): saline control, Biosorb Energy Plus (BIO), hydrochloric acid (HCl), saline + MB treated, BIO + MB treated, and HCl + MB treated. Saline, BIO, and HCl were injected into the lungs in a volume of 2 mL/kg. After surgical procedure, MB was administered intraperitoneally for 7 days at a daily dose of 2 mg/kg per day. Seven days later, rats were killed, and both lungs in all groups were examined biochemically and histopathologically. RESULTS: Our findings show that MB inhibits the inflammatory response reducing significantly (P < 0.05) peribronchial inflammatory cell infiltration, alveolar septal infiltration, alveolar edema, alveolar exudate, alveolar histiocytes, interstitial fibrosis, granuloma, and necrosis formation in different pulmonary aspiration models. Pulmonary aspiration significantly increased the tissue hydroxyproline content, malondialdehyde levels, and decreased (P < 0.05) the antioxidant enzyme (superoxide dismutase and glutathione peroxidase) activities. MB treatment significantly (P < 0.05) decreased the elevated tissue hydroxyproline content and malondialdehyde levels and prevented the inhibition of superoxide dismutase and glutathione peroxidase (P < 0.05) enzymes in the tissues. Furthermore, there is a significant reduction in the activity of inducible nitric oxide synthase (iNOS), terminal deoxynucleotidyl transferase dUTP nick end labeling, and arise in the expression of surfactant protein D in lung tissue of different pulmonary aspiration models with MB therapy. CONCLUSIONS: MB treatment might be beneficial in lung injury and therefore shows potential for clinical use.

Trophoblast Cell Proliferation and Apoptosis in Placental Development During Early Gestation Period in Rats.

OBJECTIVE: To show apoptotic and mitotic activities in differentiation and proliferation of the trophoblast through the techniques of immunohistochemistry and terminal deoxynucleotidyl transferase-mediated deoxy-uridine triphosphate-biotin nick end labeling (TUNEL), apart from achieving a morphological examination of placental development during early gestation in rats. STUDY DESIGN: Animals were sacrificed on days 7, 9, 11, and 13 of pregnancy. The samples removed from those rats were processed for purposes of microscopic analysis. The decidual structure resulting from the differentiation of the endometrial stromal cells in the uterus on days 7, 9, and 11 of pregnancy was determined. RESULTS: It was observed that the placenta, with an increasing trophoblast proliferation and differentiation, matures on day 13 of pregnancy, after which time the growth seems to be continuous. Density of PCNA-positive cells and PCNA immunostaining was observed to decrease in parallel with the age of pregnancy. The excessive number of apoptotic cells seen in the early periods of pregnancy decreased as the placenta matured. CONCLUSION: We speculate that the rat placenta grows to maturity by day 13 of pregnancy along with increased proliferation and apoptosis in the early days of pregnancy. In addition, a significant decrease of proliferation and apoptosis was observed in the placenta with increasing age of the pregnancy.

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.

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.

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.