Capsaicin prevents radiotherapy-induced premature ovarian failure in rats.

Ionising radiation exposure of 5-10gray (Gy) to the pelvic area induces premature ovarian failure (POF). Twenty-four young adult Wistar albino female rats were were treated with subcutaneous capsaicin 0.5mg/kg per day or placebo for 10days then exposed to whole body irradiation. Rats were randomly divided into four groups: (1) control; (2) capsaicin; (3) radiation only (IR): rats were injected with placebo before exposure to a single dose of 8.3-Gy whole body irradiation; (4) radiation-capsaicin (IR+CAP): rats were injected with capsaicin prior to whole body irradiation. Radiation triggered oxidative stress, increased ovarian inflammation, increased follicular apoptosis and diminished ovarian follicle pool. Capsaicin significantly ameliorated oxidative stress by decreasing serum total oxidant status, oxidative stress index, disulphide, and malondialdehyde levels (P ≤0.001); ovarian inflammatory status by decreasing expressions of TNF-α, IL-1ß, PARP-1 (P =0.002); apoptosis by decreasing expressions of active caspase-3 and p53 (P =0.015, P =0.002); and follicle counts by increasing primordial follicles and decreasing apoptotic follicles (P ≤0.001) in rats when administered before radiation exposure. The beneficial effects of capsaicin are demonstrated for the first time on ionising radiation exposed rat ovaries. Capsaicin pre-treatment before radiotherapy restores the primordial follicle pool, inhibits atresia of ovarian follicles and may be an acceptable therapeutic modality to prevent radiation-induced POF.

The potential of Raman and FT-IR spectroscopic methods for the detection of chlorine in human nail samples.

Although chlorine (Cl2) has been used as a chemical warfare agent since World War I there is no known specific and reliable biomarker to indicate the presence of chlorine. We distinguished chlorinated human nails from unchlorinated ones using Raman spectroscopy and Fourier Transform Infrared (FT-IR) Spectroscopy. This research was carried out between October 2018 and July 2019 on two nail samples taken from 55 male and 104 female volunteers. One sample from each participant was chlorinated, while the second sample was used as a control. Spectral data were collected from chlorinated and unchlorinated (control) human nails using Raman and FT-IR spectroscopy. Raman measurements were made between 100 and 3200 cm-1, while FT-IR measurements were recorded over the range of 650 to 4000 cm-1. Partial least squares regression-discriminant analysis (PLS-DA) was used to develop classification models for each spectral instrument. Results showed that the control and chlorinated nail samples were successfully discriminated with similar results achieved with both instruments. Minor differences were observed in the performance of classification models. The FT-IR spectroscopy model (sensitivity = 95%, specificity = 99%, accuracy = 97%) was found to be more successful with a smaller margin of error (sensitivity = 95%, specificity = 99%, accuracy = 96%) compared to the Raman spectroscopy model. This method can be used successfully for both ante-mortem and post-mortem diagnosis of chlorine exposure.

Evaluation of preventive effect of shilajit on radiation-induced apoptosis on ovaries.

PURPOSE: Canc er is the second leading cause of death in children in developed countries and most of childhood malignancies can be treated with chemo-radiotherapy. Although radiation therapy is a successful treatment modality in cancer patients, it has various adverse effects. Especially the gonads are very sensitive and prone to radiation-related damage. Radiation impairs the ovaries by triggering apoptosis of follicular cells and chromosomal damage and oxidative stress. Shilajit, a traditional medicinal agent in India, Russia, and other parts of the world, contains various antioxidant agents and has ovogenic effects. To evaluate the ability of shilajit to prevent radiation-induced ovarian damage. METHODS: Forty Wistar albino female rats were divided into four groups as: Control group, shilajit group, radiation only group, and radiation + shilajit group. Four days after radiation exposure, the rats were sacrificed and the ovaries were removed and evaluated immuno-histopathologically. RESULTS: There was a statistically significant difference in follicle counts (primordial, primary, preantral, antral, and atretic follicles) between the groups (p < 0.001). Almost all follicles at all stages were atretic in the radiation only group whereas normal-looking primordial follicles were detected in the radiation + shilajit group. In radiation + shilajit group, p53, Bax and caspase 3 expression was less intense than that in the radiation only group follicles. CONCLUSION: This is the first reported study evaluating the effects of shilajit on radiation-related ovarian damage prevention. Shilajit decreased the expression of p53, Bax, and caspase 3, thereby blocking the apoptotic pathways. Shilajit was found to be especially protective of primordial follicles.

The Effects of the Angiotensin Converting Enzyme Inhibitor Enalapril and the Angiotensin II Type 1 Receptor Blocker Losartan on Fracture Healing in Rats.

PURPOSE: Angiotensin converting enzyme inhibitors (ACEI) and type I angiotensin receptor blockers (ARB) have been shown to exert significant effects on bone tissue via a local renin-angiotensin-aldosterone system (RAS). The aim of our study was to delineate their influences on fracture healing process. METHODS: Sixty adult male Wistar Albino rats were divided into three groups. After undergoing surgical femoral fracture and fixation, the ACEI group received 10 mg/kg of Enalapril, the ARB group received 10 mg/kg of Losartan and the Control group did not receive any medication. Fracture healing was evaluated at second and fifth postoperative weeks by the Lane-Sandhu radiological staging system and by histological scoring system of Huoet al. ACE expression in fracture callus was studied by immunohistochemistry. RESULTS: Both ACEI and ARB groups showed less fibrous tissue in the fracture area at the second week, but the histologic score differences were significant only between Control and ARB groups. At the fifth week, however, both radiological and histological scores for the ACEI group were significantly higher than both ARB and Control groups, while the scores for ARB and Control groups were similar. The presence of ACE expression in fracture callus was also observed. CONCLUSION: ACEIs had significant positive effects on fracture repair. Losartan failed to display these stimulatory effects, which suggests that local RAS in bone tissue exerts its actions via alternative receptors or pathways than the AT1 receptor.

Protective effect of curcumin on testicular damage caused by carbon tetrachloride exposure in rats.

Context Carbon tetrachloride (CCl4 ) is a chemical that is still widely used in industry and has been shown to cause structural defects in rat testicles through oxidative stress. Aims In our study, the effect of curcumin on CCl4 -mediated testicular damage was investigated. Methods Twenty-four adult Wistar albino male rats weighing 300-350g were divided into four groups: control group (olive oil was applied by gavage every consecutive day for 3weeks); curcumin and CCl4 +curcumin groups (200mg/kg curcumin dissolved in olive oil was given by gavage once a day, every consecutive day for 3weeks); and CCl4 and CCl4 +curcumin groups (0.5mL/kg CCl4 was dissolved in olive oil at a ratio of 1/1 and given by i.p. injection every other day for 3weeks). Tissue samples were examined histopathologically, histomorphometrically, immunohistochemically and biochemically. Key results CCl4 disrupted both testicular morphology and testosterone synthesis, whereas curcumin treatment resulted in an improvement in testicular morphology and biochemical parameters, as well as a decrease in caspase-3 and tumour necrosis factor-α expression. Conclusions Curcumin has a protective effect on testicular tissue damage caused by CCl4 with its anti-inflammatory, antiapoptotic and antioxantioxidant properties. Implications Curcumin can prevent testicular damage due to CCl4 , an environmental pollutant.

Vitamin E modulates apoptosis and c-jun N-terminal kinase activation in ovarian torsion-detorsion injury.

The aim of this study was to evaluate the role of vitamin E in follicular degeneration and to assess histopathological and biochemical changes following ischemia-reperfusion (IR) injury in rat ovaries. Twenty-eight Wistar albino rats were randomly divided into four groups: sham, 4h torsion, 24h detorsion, and a vitamin E group. Thirty minutes before detorsion, a single dose of 200mg/kg vitamin E was administered intraperitoneally. The ovarian histology score was determined, serum levels of malondialdehyde (MDA) and myeloperoxidase (MPO) were measured. The apoptosis of granulosa cells and the phospho-c-jun N-terminal kinase (p-JNK) and phospho-p38 (p-p38) immunoreactivities of these cells were determined. MDA and MPO levels were significantly increased in the torsion and detorsion groups. Hemorrhage, edema, and congestion were also apparent in these groups. In addition, the apoptotic index and the immunoreactivity of p-JNK were highest in the detorsion group, which also showed marked follicular degeneration. However, p-p38 activity was not affected by torsion-detorsion (TD) induction. Vitamin E ameliorated TD-induced histological alterations. It also decreased serum levels of MDA and MPO, reduced the activity of p-JNK in the ovaries, and reduced numbers of apoptotic follicular cells. In conclusion, these data indicate that vitamin E attenuated ovarian follicular degeneration by inhibiting the immunoreactivity of p-JNK and reducing the apoptosis of granulosa cells.

The effects of human amnion membrane-derived mesenchymal stem cells conditioned medium on ionizing radiation-induced premature ovarian failure and endoplasmic reticulum stress-related apoptosis mechanism.

OBJECTIVES: Premature ovarian failure (POF) is defined as the cessation of menstrual periods for at least 4-6 months before the age of 40 years, accompanied by FSH values measuring over 40 IU/L for a month. Radiation therapy, one of the cancer treatment methods, is known to accelerate ovarian aging by reducing and eliminating the number of primordial follicles in the ovarian follicle pool. Ionizing radiation has been reported to cause POF. The objective of this study is to investigate the impact of mesenchymal stem cell conditioned medium (hAMSCs-CM), which is isolated from the amniotic membrane of human placenta, on premature ovarian failure (POF) caused by whole-body irradiation. The study will focus on the ER stress and apoptosis mechanisms in the process. STUDY DISAYN: A POF model was created by exposing rats to 7 Gy of whole-body irradiation. Serum-free hAMSCs-CM were then administered via the tail vein. Follicle count was performed on the ovaries, and immunohistochemistry was used to determine the expressions of GRP78, CHOP, IRE-1, caspase-12, caspase-9, caspase-3. TUNEL was also carried out, and levels of serum FSH, LH, E2, AMH, and oxidative stress marker 8-OHdG were measured. RESULTS AND CONCLUSION: The application of hAMSCs-CM has been found to have a positive impact on follicles affected by radiation. After treatment, the number of primordial, primary, secondary, and graafian follicles, which had previously decreased due to radiation, showed an increase. Furthermore, the number of atretic follicles, which had been increasing due to radiation, showed a decrease. ER is one of the targets affected by ionizing radiation. After ionizing radiation, the expressions of ER stress-related markers and apoptosis markers increased in the ovary. After hAMSCs-CM administration, the expressions of these markers and number of TUNEL-positive cells decreased. Following irradiation, anti-mullerian hormone (AMH) and estradiol (E2) levels decreased, while follicle stimulating hormone (FSH) and luteinizing hormone (LH) levels increased. After administration of hAMSCs-CM, AMH and E2 levels increased, while FSH and LH levels decreased. Amnion membrane-derived mesenchymal stem cell conditioned medium can play a therapeutic role in ionizing radiation-induced premature ovarian failure by reducing endoplasmic reticulum stress and apoptosis.

Protective effects of L-carnitine on X irradiation-induced uterus injury via antioxidant and anti-inflammatory pathways.

PURPOSE: Ionizing radiation causes oxidative stress induced tissue damage as well as a decline in reproduction incidence. The purpose of our study was to evaluate the effects of L-carnitine on radiation-induced uterine injury. MATERIALS AND METHODS: Thirty Wistar albino rats were classified into five groups. Physiological saline was administered intraperitoneally to the control group. A single dose of 8.3 Gy whole body X-irradiation was applied to the radiation-1 and radiation-2 groups. These groups were sacrificed on the 6th hour and 4th day, respectively, after irradiation. Radiation-1 + L-carnitine and radiation-2 + L-carnitine groups received a daily dose of 200 mg/kg L-carnitine in addition to the same dose of irradiation. L-carnitine was also applied one day before and four days after irradiation. RESULTS: L-carnitine therapy partially blocks the depletion of the deep glands and radiation-induced flattening of the glandular epithelium and endometrial surface. Proinflammatory cytokines such as IL-1ß, IL-6 and TNF-α were found to be significantly expressed in the uterus tissue of irradiated mice. In the radiation groups, NFκB and PARP-1 expressions in uterine tissue was significantly increased compared to L-carnitine treated and the control groups. It was observed that the oxidative stress index increased in the radiation groups, but decreased in the L-carnitine applied groups. CONCLUSIONS: Our findings showed that L-carnitine has a positive effect on radiation-induced uterine damage. L-carnitine may be a potential safe radio protective agent during radiotherapy for pelvic cancer provided the tumor is not protected from radiation damage to the same extent as the normal tissue is. However, prospective clinical trial studies are necessary to understand its efficacy.

Human Amnion Membrane-Derived Mesenchymal Stem Cells and Conditioned Medium Can Ameliorate X-Irradiation-Induced Testicular Injury by Reducing Endoplasmic Reticulum Stress and Apoptosis.

Today, infertility affects 15% of couples and half of this rate is due to reproductive problems in men. Radiation-induced damage to the testicles causes sterility depending on the dose. Radiation causes endoplasmic reticulum (ER) stress and ER stress induces apoptosis. In this study, the effect of human amniotic membrane-derived mesenchymal stem cells (hAMSCs) and conditioned medium (hAMSCs-CM) on testicular damage induced by ionizing radiation is aimed to be elucidated through ER stress and apoptosis mechanisms. Six gray scrotal irradiation was used to create a testicular injury model. hAMSCs isolated and characterized with immunofluorescence and flow cytometry, while 2.5 × 105 hAMSCs were transplanted into testis and hAMSCs-CM was applied. Fertility assessment was performed. Expressions of ER stress markers GRP78, Ire1, Chop and Caspase-12, and Caspase-3 were determined. TUNEL was performed. Serum FSH, LH, and testosterone were measured. After hAMSC transplantation and administration of hAMSCs-CM, offsprings were obtained. Seminiferous tubule diameter and seminiferous epithelial height increased. The expression of GRP78, IRE1α, CHOP, Caspase-12, and Caspase-3 decreased. Percentages of tunel positive cells decreased. While FSH and LH levels decreased, testosterone increased. After irradiation, both hAMSCs transplantation and paracrine activity of hAMSCs may have a role in reducing ER stress by suppressing the UPR response. Decrease in FSH and LH and increase in testosterone level after MSCs transplantation may have contributed to the improvement of spermatogenesis. Thus, it can be said that MSCs derived from human amniotic membrane can improve ionized radiation-induced testicular damage by reducing ER stress and apoptosis.

Protective effect of flaxseed oil on renal injury in hyperlipidaemic rats: the effect of flaxseed oil on hyperlipidaemia.

This study evaluated the possible effects of flaxseed oil on renal damage associated with hyperlipidaemic rats. Wistar albino male rats were divided into three groups. Group I was fed with a pellet chow. Group II was fed with a high cholesterol diet (HCD) consisting of 5% cholesterol and 0.35% cholic acid added to the pellet chow. Group III was fed with the same HCD, but were orally treated with a dose of 15 mg/kg body wt/day flaxseed oil. Flaxseed oil treatment started 1 week before and continued throughout the 22 weeks of the HCD. At the end of the experiment, renal tissue and blood samples were collected. The biochemical and histopathological findings confirmed renal damage in hypercholesterolaemia conditions. Flaxseed oil reduced the hypercholesterolaemia-induced increase in the serum levels of total cholesterol, LDL and urea. Oil red O stain revealed that lowered serum lipid was accompanied by a decreased deposition of neutral lipid. Flaxseed oil effectively reversed these abnormalities, verifying the protective effects of flaxseed oil in ameliorating renal injuries associated with hypercholesterolaemia.

X irradiation induced colonic mucosal injury and the detection of apoptosis through PARP-1/p53 regulatory pathway.

This study aimed to explore whether PARP-1 regulatory pathway mediated X irradiation induced cell cycle arrest and apoptosis or not. In this regard, colonic mucosal injury caused by whole-body X-irradiation induced apoptosis through PARP-1, caspase 3 and p53 regulatory pathway were evaluated in experimental rat models. Eighteen Wistar albino rats were divided into three groups. Two radiation groups received 8.3 Gy dose of whole-body X-irradiation as a single dose and the control group received physiological saline intraperitoneally. Radiation groups were sacrificed after 6 h and 4 days of irradiation. PARP-1 and caspase 3 expression in the nuclei of colonic crypt cells significantly increased 6 h after irradiation, and declined 4 days after irradiation. In conflict with other studies that reported p53 as not being expressed widely in colonic mucosa, in our study the expressions of p53 were elevated both in the cytoplasm and in the nucleus of the crypt cells, especially 6 h after irradiation. In the radiation groups, colonic mucosal injury score was significantly elevated compared with that of the control group. Our data demonstrated that PARP-1, caspase-3 and p53 expression increased in colonic mucosa 6 h after irradiation.

Protective effects of curcumin against gamma radiation-induced ileal mucosal damage.

The major objective of this study was to test curcumin as a potential radioprotectant for the ileum goblet cells of the rat. Wistar albino rats were used in the study. Group A was the control group and group B was the single dose radiation group. Group C was the two dose radiation group (4 days interval). The rats in groups D and E were given a daily dose of 100 mg/kg of curcumin for 14 and 18 days, respectively. During the curcumin administration period, the rats in group D were exposed to abdominal area gamma (gamma)-ray dose of 5 Gy on the 10th day and group E was exposed to same dose radiation on the 10th and 14th day. Irradiation and treatment groups were decapitated on the 4th day after exposure to single or two-dose irradiation and ileum tissues were removed for light and electron microscopic investigation. Single or two dose 5 Gy gamma-irradiation caused a marked intestinal mucosal injury in rats on the 4th day. Radiation produced increases in the number of goblet cells. Curcumin appears to have protective effects against radiation-induced damage, suggesting that clinical transfer is feasible.

[Rectal dexmedetomidine in rats: evaluation of sedative and mucosal effects]. / Dexmedetomidina retal em ratos: avaliação dos efeitos sedativos e sobre a mucosa.

BACKGROUND AND OBJECTIVES: In this study, we investigated the anesthetic and mucosal effects of the rectal application of dexmedetomidine to rats. METHODS: Male Wistar albino rats weighing 250-300g were divided into four groups: Group S (n=8) was a sham group that served as a baseline for the normal basal values; Group C (n=8) consisted of rats that received the rectal application of saline alone; Group IPDex (n=8) included rats that received the intraperitoneal application of dexmedetomidine (100µgkg(-1)); and Group RecDex (n=8) included rats that received the rectal application of dexmedetomidine (100µgkg(-1)). For the rectal drug administration, we used 22G intravenous cannulas with the stylets removed. We administered the drugs by advancing the cannula 1cm into the rectum, and the rectal administration volume was 1mL for all the rats. The latency and anesthesia time (min) were measured. Two hours after rectal administration, 75mgkg(-1) ketamine was administered for intraperitoneal anesthesia in all the groups, followed by the removal of the rats' rectums to a distal distance of 3cm via an abdominoperineal surgical procedure. We histopathologically examined and scored the rectums. RESULTS: Anesthesia was achieved in all the rats in the Group RecDex following the administration of dexmedetomidine. The onset of anesthesia in the Group RecDex was significantly later and of a shorter duration than in the Group IPDEx (p<0.05). In the Group RecDex, the administration of dexmedetomidine induced mild-moderate losses of mucosal architecture in the colon and rectum, 2h after rectal inoculation. CONCLUSION: Although 100µgkg(-1) dexmedetomidine administered rectally to rats achieved a significantly longer duration of anesthesia compared with the rectal administration of saline, our histopathological evaluations showed that the rectal administration of 100µgkg(-1) dexmedetomidine led to mild-moderate damage to the mucosal structure of the rectum.

N-Acetylcysteine counteracts oxidative stress and protects alveolar epithelial cells from lung contusion-induced apoptosis in rats with blunt chest trauma.

The aim of this study was to investigate the protective effects of N-acetylcysteine (NAC) on peroxidative and apoptotic changes in the contused lungs of rats following blunt chest trauma. The rats were randomly divided into three groups: control, contusion, and contusion + NAC. All the rats, apart from those in the control group, performed moderate lung contusion. A daily intramuscular NAC injection (150 mg/kg) was given immediately following the blunt chest trauma and was continued for two additional days following cessation of the trauma. Samples of lung tissue were taken in order to evaluate the tissue malondialdehyde (MDA) level, histopathology, and epithelial cell apoptosis using terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) assay and active caspase-3 immunostaining. In addition, we immunohistochemically evaluated the expression of surfactant protein D (SP-D) in the lung tissue. The blunt chest trauma-induced lung contusion resulted in severe histopathological injury, as well as an increase in the MDA level and in the number of cells identified on TUNEL assay together with active caspase-3 positive epithelial cells, but a decrease in the number of SP-D positive alveolar type 2 (AT-2) cells. NAC treatment effectively attenuated histopathologic, peroxidative, and apoptotic changes, as well as reducing alterations in SP-D expression in the lung tissue. These findings indicate that the beneficial effects of NAC administrated following blunt chest trauma is related to the regulation of oxidative stress and apoptosis.

Protection by L-carnitine against radiation-induced ileal mucosal injury in the rat: pattern of oxidative stress, apoptosis and cytokines.

PURPOSE: In this study, we tested the effects of L-carnitine (LC) on radiation-induced ileal mucosal damage. MATERIALS AND METHODS: Thirty Wistar albino rats were divided into five groups. The control group received physiological saline intraperitoneally (i.p.). Radiation-1 and radiation-2 groups received whole-body X-irradiation of 8.3 Gy as a single dose. These groups were sacrificed at the 6th hour and 4th day after irradiation, respectively. The Radiation-1 + LC and the radiation-2 + LC groups received the same dose irradiation plus a daily dose of 200 mg/kg LC. LC was applied one day before and for four days after irradiation. RESULTS: The levels of serum monocyte chemotactic protein-1 (MCP-1) and interferon gamma (IFN-γ) were significantly higher in the radiation groups when compared with the control. Treatment with LC decreased the serum MCP-1 and IFN-γ levels considerably. In the radiations groups, the Chiu score was significantly elevated compared with that of the control group. However, LC administered prior to the irradiation reduced the severity of mucosal damage. The number of apoptotic cells of the ileal crypt in the irradiated rats increased from the 6th hour after irradiation and then decreased at 4th day. CONCLUSIONS: Our data demonstrated that LC may be beneficial to radiation enteritis.

Effects of curcumin on apoptosis and oxidoinflammatory regulation in a rat model of acetic acid-induced colitis: the roles of c-Jun N-terminal kinase and p38 mitogen-activated protein kinase.

The present study evaluated the effects of curcumin on epithelial cell apoptosis, the immunoreactivity of the phospho-c-Jun N-terminal kinase (JNK) and phospho-p38 mitogen-activated protein kinases (MAPKs) in inflamed colon mucosa, and oxidative stress in a rat model of ulcerative colitis induced by acetic acid. Rats were randomly divided into three groups: control, acetic acid, and acetic acid+curcumin. Curcumin (100 mg/kg per day, intragastrically) was administered 10 days before the induction of colitis and was continued for two additional days. Acetic acid-induced colitis caused a significant increase in the macroscopic and microscopic tissue ranking scores as well as an elevation in colonic myeloperoxidase (MPO) activity, malondialdehyde (MDA) levels, and the number of apoptotic epithelial cells in colon tissue compared to controls. In the rat colon, immunoreactivity of phospho-p38 MAPK was increased, whereas the phospho-JNK activity was decreased following the induction of colitis. Curcumin treatment was associated with amelioration of macroscopic and microscopic colitis sores, decreased MPO activity, and decreased MDA levels in acetic acid-induced colitis. Furthermore, oral curcumin supplementation clearly prevented programmed cell death and restored immunreactivity of MAPKs in the colons of colitic rats. The results of this study suggest that oral curcumin treatment decreases colon injury and is associated with decreased inflammatory reactions, lipid peroxidation, apoptotic cell death, and modulating p38- and JNK-MAPK pathways.

Protective effect of sildenafil on liver injury induced by intestinal ischemia/reperfusion.

BACKGROUND: This study evaluated the protective effect of sildenafil on liver injury induced by intestinal ischemia-reperfusion. METHODS: Forty female Sprague Dawley rats were divided into 4 groups: sham-control (SC), ischemia (I), ischemia-reperfusion (IR), and ischemia-reperfusion+sildenafil (SIL; sildenafil gavaged at 50mg/kg before operating). A 2-h ischemia-reperfusion was performed by clamping the superior mesenteric artery. Liver function, plasma alanine (ALT) and aspartate (AST) aminotransferase, and intestinal and liver malondialdehyde (MDA) were measured at the end of the experiment. Intestinal and liver tissue damage was examined by histology. Liver samples were immunologically stained for endothelial nitric oxide synthase (eNOS) and proliferating cell nuclear antigen (PCNA). RESULTS: The ALT and AST levels were highest in the IR group and were lower in the SIL group (p<0.05). Intestinal MDA levels were statistically higher in the IR group than in the SC, I and SIL groups. Liver MDA levels were significantly higher in the IR group than in the I and SC groups (p<0.05) and higher than in the SIL group (p>0.05). Intestinal damage based on Chiu scoring was more severe in the IR than in the SIL group (p<0.05). Sildenafil reduced damage and also increased eNOS and PCNA immunoreactivity in liver tissue. CONCLUSIONS: Sildenafil shows a protective effect on intestinal ischemia-reperfusion-induced liver injury, possibly by decreasing vascular resistance through increased nitric oxide levels.

The Protective Effect of Curcumin on Ionizing Radiation-induced Cataractogenesis in Rats.

OBJECTIVE: The aim of the study was to determine the protective effect of curcumin against ionizing radiation-induced cataract in the lens of rats. MATERIAL AND METHODS: Rats were divided into six groups. Group 1: Control, Group 2: Dimethyl sulfoxide (DMSO), Group 3: DMSO+curcumin, Group 4: Irradiation, Group 5: Irradiation+DMSO, Group 6: Irradiation+DMSO+curcumin. A 15 Gy total dose was given to 4, 5, 6 groups for radiation damage. Curcumin (100 mg/kg) was dissolved in DMSO and given by intragastric intubation for 28 days. At the end of the experiment, lenses were graded and enucleated. The lenticular activity of the antioxidant enzymes, total antioxidant and glutathione peroxidase (GSH-Px), and the malondialdehyde (MDA) were measured. RESULTS: 100% Cataract was seen in the irradiation group. Cataract rate fell to 40% and was limited at grade 1 and 2 in the curcumin group. In the irradiation group, antioxidant enzyme levels were decreased, MDA levels were increased. There was an increase in antioxidant enzyme levels and a significant decrease in MDA in the group which was given curcumin. CONCLUSION: Curcumin has antioxidant and radioprotective properties and is likely to be a valuable agent for protection against ionizing radiation. Hence, it may be used as an antioxidant and radioprotector against radiation-induced cataractogenesis.

Rectal dexmedetomidine in rats: evaluation of sedative and mucosal effects / Dexmedetomidina retal em ratos: avaliação dos efeitos sedativos e sobre a mucosa / La dexmedetomidina rectal en ratones: evaluación de los efectos sedativos y sobre la mucosa

BACKGROUND AND OBJECTIVES: In this study, we investigated the anesthetic and mucosal effects of the rectal application of dexmedetomidine to rats. METHODS: Male Wistar albino rats weighing 250-300 g were divided into four groups: Group S (n = 8) was a sham group that served as a baseline for the normal basal values; Group C (n = 8) consisted of rats that received the rectal application of saline alone; Group IPDex (n = 8) included rats that received the intraperitoneal application of dexmedetomidine (100 µg kg-1); and Group RecDex (n = 8) included rats that received the rectal application of dexmedetomidine (100 µg kg-1). For the rectal drug administration, we used 22 G intravenous cannulas with the stylets removed. We administered the drugs by advancing the cannula 1 cm into the rectum, and the rectal administration volume was 1 mL for all the rats. The latency and anesthesia time (min) were measured. Two hours after rectal administration, 75 mg kg-1 ketamine was administered for intraperitoneal anesthesia in all the groups, followed by the removal of the rats' rectums to a distal distance of 3 cm via an abdominoperineal surgical procedure. We histopathologically examined and scored the rectums. RESULTS: Anesthesia was achieved in all the rats in the Group RecDex following the administration of dexmedetomidine. The onset of anesthesia in the Group RecDex was significantly later and of a shorter duration than in the Group IPDEx (p < 0.05). In the Group RecDex, the administration of dexmedetomidine induced mild-moderate losses of mucosal architecture in the colon and rectum, 2 h after rectal inoculation. CONCLUSION: Although 100 µg kg-1 dexmedetomidine administered rectally to rats achieved a significantly longer duration of anesthesia compared with the rectal administration of saline, our histopathological evaluations showed that the rectal administration of 100 µg kg-1 dexmedetomidine led to mild-moderate damage to the mucosal structure ...

JUSTIFICATIVA E OBJETIVOS: Neste estudo pesquisamos os efeitos anestésicos e sobre a mucosa da aplicação retal de dexmedetomidina em ratos. MÉTODOS: Ratos machos albinos Wistar, com 250-300 g, foram divididos em quatro grupos: Grupo S (n = 8) foi um grupo sham que serviu de parâmetro para os valores basais normais; Grupo C (n = 8) consistiu em ratos que receberam a aplicação retal apenas de soro fisiológico; Grupo IPDex (n = 8) consistiu em ratos que receberam aplicação intraperitoneal de dexmedetomidina (100 µg kg-1) e Grupo RecDex (n = 8) consistiu em ratos que receberam a aplicação retal de dexmedetomidina (100 µg kg-1). Para a administração dos fármacos por via retal, usamos cânulas intravenosas de calibre 22, com os estiletes removidos. A administração consistiu em avançar a cânula 1 cm no reto e o volume de administração retal foi de 1 mL para todos os ratos. Os tempos (min) de latência e de anestesia foram registrados. Duas horas após a administração por via retal, 75 mg kg-1 de cetamina foram administrados a todos os grupos para anestesia intraperitoneal, seguido por remoção dos retos dos ratos a uma distância 3 cm distal por meio de procedimento cirúrgico abdominoperineal. Os retos foram histopatologicamente examinados e classificados. RESULTADOS: A anestesia foi feita em todos os ratos do grupo RecDex após a administração de dexmedetomidina. O tempo de início da anestesia no Grupo RecDex foi significativamente mais longo e com uma duração mais curta do que no Grupo IPDEx (p < 0,05). No Grupo RecDex, a administração de dexmedetomidina induziu perdas leves a moderadas da arquitetura da mucosa do cólon e reto duas horas após a inoculação retal. CONCLUSÃO: Embora a administração de 100 µg kg-1 de dexmedetomidina por via retal em ratos tenha resultado em uma duração significativamente maior da anestesia, em comparação com a administração retal de soro fisiológico, nossas avaliações histopatológicas mostraram que a administração ...

JUSTIFICACIÓN Y OBJETIVOS: En este estudio investigamos los efectos anestésicos y sobre la mucosa de la aplicación rectal de la dexmedetomidina en los ratones. MÉTODOS: Ratones machos albinos Wistar, con un peso de 250-300 g, fueron divididos en 4 grupos: el grupo S (n = 8) fue un grupo simulado que sirvió de base para los valores basales normales; el grupo C(n = 8) consistió en ratones que recibieron aplicación rectal solamente de suero fisiológico; el grupo IPDex (n = 8) estaba formado por en ratones que recibieron aplicación intraperitoneal de dexmedetomidina (100 µg/kg-1); y el grupo RecDex (n = 8) consistió en ratones que recibieron la aplicación rectal de dexmedetomidina (100 µg/kg-1). Para la administración de los fármacos por vía rectal usamos cánulas intravenosas de calibre 22 sin estiletes. La administración consistió en avanzar la cánula 1 cm en el recto y el volumen de administración rectal fue de 1 mL para todos los ratones. Los tiempos (min) de latencia y de anestesia fueron registrados. Dos horas después de la administración por vía rectal, fueron administrados 75 mg/kg-1 de ketamina a todos los grupos para la anestesia intraperitoneal, seguido de la retirada de los rectos de los ratones a una distancia 3 cm distal por medio de un procedimiento quirúrgico abdominoperineal. Los rectos fueron histopatológicamente examinados y clasificados. RESULTADOS: La anestesia fue realizada en todos los ratones del grupo RecDex después de la administración de dexmedetomidina. El inicio de la anestesia en el grupo RecDex fue significativamente más tarde y con una duración más corta que en el grupo IPDEx (p < 0,05). En el grupo RecDex, la administración de dexmedetomidina indujo pérdidas leves a moderadas de la arquitectura de la mucosa del colon y del recto 2 h después de la inoculación rectal. CONCLUSIÓN: Aunque la administración de 100 µg/kg-1 de dexmedetomidina por vía rectal en ratones logra una duración significativamente más ...

Protective effects of the volatile oil of Nigella sativa seeds on beta-cell damage in streptozotocin-induced diabetic rats: a light and electron microscopic study.

The aim of this study was to evaluate the possible protective effects of the volatile oil of Nigella sativa (NS) seeds on insulin immunoreactivity and ultrastructural changes of pancreatic beta-cells in STZ-induced diabetic rats. STZ was injected intraperitoneally at a single dose of 50 mg/kg to induce diabetes. The rats in NS treated groups were given NS (0.2 ml/kg) once a day orally for 4 weeks starting 3 days prior to STZ injection. To date, no ultrastructural changes of pancreatic beta-cells in STZ induced diabetic rats by NS treatment have been reported. Islet cell degeneration and weak insulin immunohistochemical staining was observed in rats with STZ-induced diabetes. Increased intensity of staining for insulin, and preservation of beta-cell numbers were apparent in the NS-treated diabetic rats. The protective effect of NS on STZ-diabetic rats was evident by a moderate increase in the lowered secretory vesicles with granules and also slight destruction with loss of cristae within the mitochondria of beta-cell when compared to control rats. These findings suggest that NS treatment exerts a therapeutic protective effect in diabetes by decreasing morphological changes and preserving pancreatic beta-cell integrity. Consequently, NS may be clinically useful for protecting beta-cells against oxidative stress.