The Impact of Complex Loadings on the Structure of the L2-L3 Intervertebral Disc in a Sheep Spine Cadaver Model: A Biomechanical and Histological Evaluation.

Background The human vertebral column generates movements under versatile, dynamic loads. Understanding how the spine reacts to these movements and loads is crucial for developing new spine implants and surgical treatments for intervertebral disc injuries. Mechanically uni-axial compression models have been extensively studied. However, the spine's daily loading is not limited to compression, so it is crucial to measure its behavior in all movements (flexion-extension, rotation, and axial compression). Methods This study utilized L1-L5 segments from 19 healthy adult sheep spines. The L2-L3 disc of the first spine underwent only histological evaluation without biomechanical testing to define basic histological parameters. The remaining 18 were divided into three groups of six and subjected to biomechanical tests. Different mechanisms for three groups of spinal segments were prepared, and tests were performed on Shimadzu AG-IS 10 KN (Universal Drawing Press, Kyoto, Japan). An axial load (800 N) was applied to the first group, an axial load with 15 degrees of flexion to the second group, and an axial load with 10 degrees of rotation plus 15 degrees of flexion to the third group. A biomechanical evaluation of the maximum elongation amounts (MEAs) was performed and compared between the groups. Then, the L2-L3 discs were removed from the sheep spines, and a histological examination of the discs was conducted using Hematoxylin-Eosin (HE), Alcian Blue (AB), and Masson's Trichrome (MT) staining. Results The mean MEA ± Standard Deviation (Range) was 1.39 ± 0.38 (0.91-1.94) for Group 1, 2.02 ± 0.75 (0.91-3.01) for Group 2, and 2.47 ± 1.09 (0.64-3.9) for Group 3. Biomechanically, although MEAs increased from Group 1 to Group 3 (meaning that the mean MEAs increased as the number of types of applied force increased), there was no statistically significant difference between the groups regarding the MEAs (P = 0.092). Histologically, no significant differences were observed between all groups after HE staining. In all groups, hypercellularity, edema in the connective tissue, separation between tissue layers, delamination, and signs of swelling and necrosis in the cells were observed similarly. For the AB staining, there was a decrease in the glycosaminoglycan (GAG) structure in the tissue samples compared to the control tissue, but no significant differences were observed between the groups. However, it was observed that the stratification in Group 3 was slightly more deteriorated than in the other groups. For the MT staining, collagen structure deterioration was observed in all groups. It was observed that the amount of collagen was significantly reduced compared to the control tissue. Conclusion As a result, when the axial load is applied biomechanically, there is more displacement of the vertebral discs in Group 3 with multidimensional movements. Furthermore, histological studies revealed deterioration between tissue layers when exposed to complex movements, and the degradation of stratification in group 3 compared to other loading combinations in groups 2 and 3 may indicate the role of complex loads in the formation of disc herniation.

Addition of Transfixation Suture to Purse String Suture During Intraperitoneal Inguinal Hernia Repair Increases Peri-Hernia Sac Neck Collagen Formation.

BACKGROUND: The worldwide accepted repair for indirect inguinal hernia in children is high ligation of the hernia sac with open herniotomy. However, laparoscopic pediatric inguinal hernia repair (IHR) has been gaining popularity in the last two decades. An experimental study was conducted to investigate the effects of different intraperitoneal IHR suture techniques on the collagen formation at the hernia sac neck. METHODS: Present study was conducted on thirty-five male adult (3-6 months old) Wistar-Albino rats (260-300 g). Intraperitoneal IHR with different hernia sac neck suturing techniques (purse string suture only, transfixation suture only and purse string suture plus transfixation suture) were performed through median laparotomy using open operative techniques. Non-absorbable 2/0 braided polyester suture with 16 mm 1/2 curved round needle (Ti-cron, Covidien, MN) was used as suture material. RESULTS: The highest collagen thickness around the suture was detected in intraperitoneal IHR with purse-string plus transfixation suture group. The collagen thickness of the intraperitoneal IHR with purse string suture only and IHR with tranfixation suture only groups were not statistically significantly different. The collagen thickness of the intraperitoneal IHR with purse string suture plus transfixation suture group was statistically significantly higher compared with the intraperitoneal IHR with purse string suture only and intraperitoneal IHR with transfixation suture only groups. CONCLUSIONS: The combined usage of purse string suture and transfixation suture during laparoscopic intraperitoneal inguinal hernia repair further stimulates mesothelial fibrosis at the hernia sac neck compared with mesothelial fibrosis induced by purse string suture only or transfixation suture only.

Effect of ferulic acid on testicular damage caused by torsion-detorsion in rats.

Testicular torsion is twisting of the spermatic cord around its axis, which impairs blood flow and causes ischemia and formation of free radicals. Ferulic acid is a phenolic acid of the hydroxycinnamic family that is found in the seeds and leaves of plants; it is present in substantial amounts in fruits and vegetables. We investigated the protective effect of ferulic acid on experimental testicular torsion in rats. Animals were divided randomly into five groups: control, ethyl alcohol, torsion, torsion-detorsion, and torsion-detorsion + ferulic acid. Histopathology was assessed using hematoxylin and eosin, and periodic acid-Schiff staining. Tissues were assessed using TUNEL, active caspase-3, myeloperoxidase and inducible nitric oxide synthase immunostaining. Biochemical changes were assessed using assays for superoxide dismutase, malondialdehyde, glutathione peroxidase and glutathione. Ferulic acid reduced the levels of free radicals and increased the levels of antioxidants. Ferulic acid also reduced histopathological changes and germ cell differentiation in the testis following torsion-detorsion. Ferulic acid should be investigated further as a potential treatment for sequelae of torsion-detorsion injury.

Effect of humic acid on oxidative stress and neuroprotection in hypoxic-ischemic brain injury: part 1.

BACKGROUND: Aimed to investigate in an animal model the efficacy of humic acid by showing its antioxidant and anti-apoptotic effect comparing with the histopathological and neurological outcomes for the hypoxic-ischemic brain injury. METHODS: 28 Wistar-Albino rats who were on the 7th postnatal day and weighting between 9 and 19 g randomly divided into four groups with developed HIE model under the gas anesthesia. 20 mg/kg and 10 mg/kg intraperitoneal HA were given to Group I and II respectively. Saline was given to Group III and the sham group was Group IV. The brain tissues were stained with cresyl-violet histochemistry for grading neuronal cell injury and caspase immunohistochemistry. RESULTS: The neuronal cell injury was statistically lower in all neuroanatomical lands in HA treatment groups. The degree of ischemia was significantly smaller in HA groups. Caspase-3 immunoreactivity was decreased in the HA groups compared with the saline group. When the groups were compared, there were no serious neuronal injury in Group I. CONCLUSIONS: This is the first study which investigates the role of HA in HIE model. HA reduces apoptosis and neuronal injury in cerebral tissue of the rats. This findings suggest that HA may be viable protective agent against HIE.

The effects of hypothyroidism and hyperthyroidism on placental Hofbauer cells of pregnant rats.

We investigated the effects of maternal thyroid disorders on Hofbauer cells of both the placenta and the fetus in pregnant rats. We divided 21 rats into three groups: control group, induced hypothyroidism (hypo) group and induced hyperthyroidism (hyper) group. Hypothyroidism was induced using propylthiouracil and hyperthyroidism was induced using L-thyroxine. We measured maternal weight, maternal free thyroxine, fetal weight, fetal viability and placental morphology. At the end of the experiment, fetuses of the hypo and hyper groups were less developed than those of the control group. In the hypo and hyper groups, the thickness of the labyrinth zone was decreased, but thickness of the basal zone and decidua basalis was increased. The number of Hofbauer cells was increased in both the hypo and hyper groups. Vascular endothelial growth factor expression was increased in both the hypo and hyper groups compared to controls. Our findings indicate that maternal thyroid disorders exert a negative effect on fetal growth and placental development.

The role of FGF-4 and FGFR-2 on preimplantation embryo development in experimental maternal diabetes.

OBJECTIVE: Diabetes mellitus can cause spontaneous abortion, neonatal diseases, congenital malformations, and death. There are many studies related to the damage of in vitro hyperglycemia on embryogenesis in literature, but not enough studies on in vivo hyperglycemia effects on embryogenesis. Fibroblast growth factor (FGF) molecules play an essential role in pre-implantation embryo development and diabetes pathogenesis. In our study, we researched whether FGF-4 and FGFR-2 were playing a role in maternal diabetes' effects on embryo development. MATERIAL AND METHODS: Thirty adult virgin female BALB/c mice were randomly divided into two groups: control and diabetic. The experimental diabetes model was generated by streptozotocin (55 mg/kg, once, intraperitoneally). The control and the diabetic group were mated. Embryos were collected at the morula and blastocyte stages corresponding to the third and fourth days of pregnancy. Embryo's FGF-4 and FGFR-2 molecules were evaluated by their immunofluorescence staining and immunoreactivity score. RESULT: The results clearly showed that the FGF-4 and FGFR-2 immunofluorescence reactivity was higher in the diabetes group. CONCLUSION: We concluded that FGF-4 and FGFR-2 overexpression might impair mouse pre-implantation embryo development in maternal diabetes and suggest investigating whether they have crucial effects on human embryo development and infertility in maternal diabetes.

The effects of resveratrol against trifluralin toxicity in the urinary tract of rats.

The herbicide itself and the degradation products are highly toxic on biological systems. The aim of this study is to investigate the potential toxic effects of trifluralin (TRF) on the urinary system of male rats and to investigate the protective effects of resveratrol (RSV) in TRF-induced urinary system damage. A total of 35 male Wistar rats were randomly divided into: (1) control group, (2) sham group, (3) low dose TRF group (0.8 g/kg/day), (4) high dose TRF group (2 g/kg/day) and (5) high dose TRF + RSV group 10 mg/kg/day. RSV was administered for 21 days by intragastric gavage at a dose of 10 mg/kg/day after induction of TRF. Kidney, ureter and urinary bladder tissue was examined using light microscopy and ultrastructurally. Terminal deoxynucleotidyl transferase-mediated dUTP nick end labelling was performed to detect apoptosis. Superoxide dismutase (SOD), glutathion peroxidase (GPx) and malondialdehyde (MDA) levels were also evaluated biochemically for oxidative stress parameters. Histological evaluation showed that TRF increases apoptosis and oxidative stress, causes histological tissue damages and biochemical changes in the kidneys but does not cause any damage to the ureter and bladder. Treatment with RSV significantly attenuated tissue damage in the urinary system of rats. Apopitotic cells were significantly decreased in the treatment group. Additionally, treatment with RSV decreased SOD and GPx levels and increased MDA levels in the kidney tissue of animals subjected to TRF. These results show that RSV can significantly minimize histological damage and biochemical differences in treating TRF-induced kidney injury in rats.

The Role of Rac1 on Carbachol-induced Contractile Activity in Detrusor Smooth Muscle from Streptozotocin-induced Diabetic Rats.

This study was designed to determine the role of the small GTPase Rac1 on carbachol-induced contractile activity in detrusor smooth muscle using small inhibitor NSC 23766 in diabetic rats. Rac1 expression in bladder tissue was also evaluated. In the streptozotocin (STZ)-induced diabetic rat model, three study groups were composed of control, diabetic and insulin-treated diabetic subjects. The detrusor muscle strips were suspended in organ baths at the end of 8-12 weeks after STZ injection. Carbachol (CCh) (10(-9) -10(-4) M) concentration-response curves were obtained both in the absence and in the presence of Rac1 inhibitor NSC 23766 (0.1, 1 and 10 µM). Diabetes-related histopathological changes and Rac1 expressions were assessed by haematoxylin and eosin staining and immunohistochemical staining, respectively. CCh caused dose-dependent contractile responses in all the study groups. Rac1 inhibitor NSC 23766 inhibited CCh-induced contractile responses in all groups, but this inhibition seen in both diabetes groups was greater than in the control group. Histological examination revealed an increased bladder wall thickness both in the diabetes and in the insulin-treated diabetes groups compared to the control group. In immunohistochemical staining, expression of Rac1 was observed to be increased in all layers of bladder in both diabetic groups compared to the control group. In the diabetic bladders, increased expression of Rac1 and considerable inhibition of CCh-induced responses in the presence of NSC 23766 compared to those of the control group may indicate a specific role of Rac1 in diabetes-related bladder dysfunction, especially associated with cholinergic mediated detrusor overactivity.

Autologous rabbit adipose tissue-derived mesenchymal stromal cells for the treatment of bone injuries with distraction osteogenesis.

BACKGROUND AIMS: Adipose tissue-derived mesenchymal stromal cells (MSCs) have a higher capacity for proliferation and differentiation compared with other cell lineages. Although distraction osteogenesis is the most important therapy for treating bone defects, this treatment is restricted in many situations. The aim of this study was to examine the therapeutic potential of adipose tissue-derived MSCs and osteoblasts differentiated from adipose tissue-derived MSCs in the treatment of bone defects. METHODS: Bone defects were produced in the tibias of New Zealand rabbits that had previously undergone adipose tissue extraction. Tibial osteotomy was performed, and a distractor was placed on the right leg of the rabbits. The rabbits were placed in control (group I), stem cell (group II) and osteoblast-differentiated stem cell (group III) treatment groups. The rabbits were sacrificed, and the defect area was evaluated by radiologic, biomechanical and histopathologic tests to examine the therapeutic effects of adipose tissue-derived MSCs. RESULTS: Radiologic analyses revealed that callus density and the ossification rate increased in group III compared with group I and group II. In biomechanical tests, the highest ossification rate was observed in group III. Histopathologic studies showed that the quality of newly formed bone and the number of cells active in bone formation were significantly higher in group III rabbits compared with group I and group II rabbits. CONCLUSIONS: These data reveal that osteoblasts differentiated from adipose tissue-derived MSCs shorten the consolidation period of distraction osteogenesis. Stem cells could be used as an effective treatment for bone defects.

Effects of lipoic acid in an experimentally induced hypertensive and diabetic rat model.

In this study, experimental diabetes and nephrectomy have been applied separately and together in order to investigate the possible therapeutic effects of lipoic acid (LA) on hypertensive and diabetic rat kidneys. Wistar rats were divided into eight groups: control, diabetes mellitus (DM), 5/6 nephrectomy, DM + 5/6 nephrectomy, LA administration, DM + LA treated, 5/6 nephrectomy + LA treated, and DM + 5/6 nephrectomy + LA-treated groups, respectively. Renal damage was evaluated histomorphometrically, ultrastructurally, and biochemically. Our findings supported that diabetes and hypertension together increased the rate of renal injury, and LA had therapeutic effects on hypertensive and diabetic rat kidneys.

Effect of Hedera helix on lung histopathology in chronic asthma.

Hedera helix is widely used to treat bronchial asthma for many years. However, effects of this herb on lung histopathology is still far from clear. We aimed to determine the effect of oral administration of Hedera helix on lung histopathology in a murine model of chronic asthma.BALB/c mice were divided into four groups; I (Placebo), II (Hedera helix), III (Dexamethasone) and IV (Control). All mice except controls were sensitized and challenged with ovalbumin. Then, mice in group I received saline, group II 100 mg/kg Hedera helix and group III 1 mg/kg dexamethasone via orogastic gavage once daily for one week. Airway histopathology was evaluated by using light and electron microscopy in all groups.Goblet cell numbers and thicknesses of basement membrane were found significantly lower in group II, but there was no statistically significant difference in terms of number of mast cells, thicknesses of epithelium and subepithelial smooth muscle layers between group I and II. When Hedera helix and dexamethasone groups were compared with each other, thickness of epithelium, subepithelial muscle layers, number of mast cells and goblet cells of group III were significantly ameliorated when compared with the group II. Although Hedera helix administration reduced only goblet cell counts and the thicknesses of basement membrane in the asthmatic airways, dexamethasone ameliorated all histopathologic parameters except thickness of basement membrane better than Hedera helix.

The effects of α-lipoic acid against testicular ischemia-reperfusion injury in Rats.

Testicular torsion is one of the urologic emergencies occurring frequently in neonatal and adolescent period. Testis is sensitive to ischemia-reperfusion injury, and, therefore, ischemia and consecutive reperfusion cause an enhanced formation of reactive oxygen species that result in testicular cell damage and apoptosis. α-lipoic acid is a free radical scavenger and a biological antioxidant. It is widely used in the prevention of oxidative stress and cellular damage. We aimed to investigate the protective effect of α-lipoic acid on testicular damage in rats subjected to testicular ischemia-reperfusion injury. 35 rats were randomly divided into 5 groups: control, sham operated, ischemia, ischemia-reperfusion, and ischemia-reperfusion +lipoic acid groups, 2 h torsion and 2 h detorsion of the testis were performed. Testicular cell damage was examined by H-E staining. TUNEL and active caspase-3 immunostaining were used to detect germ cell apoptosis. GPx , SOD activity, and MDA levels were evaluated. Histological evaluation showed that α-lipoic acid pretreatment reduced testicular cell damage and decreased TUNEL and caspase-3-positive cells. Additionally, α-lipoic acid administration decreased the GPx and SOD activity and increased the MDA levels. The present results suggest that LA is a potentially beneficial agent in protecting testicular I/R in rats.

Glycyrrhizin and long-term histopathologic changes in a murine model of asthma.

BACKGROUND: Licorice root has been widely used to treat bronchial asthma for many years. However, the effect of this herb on lung histopathologic features is not fully understood. OBJECTIVE: In this study, we aimed to determine the effects of oral administration of glycyrrhizin, an active constituent of licorice root, on lung histopathologic features in BALB/c mice, in which the model of chronic asthma was established. METHODS: Twenty-eight BALB/c mice were divided into 4 groups: control, placebo, dexamethasone, and glycyrrhizin. Mice in the treatment and placebo groups were sensitized with 2 intraperitoneal injections of ovalbumin and then were exposed to aerosolized ovalbumin for 30 minutes per day on 3 days each week for 8 weeks beginning on the 21st study day. In the last week of inhalational exposure, mice in the placebo group received saline and those in the treatment groups received either dexamethasone, 1 mg/kg, or glycyrrhizin, 10 mg/kg, via orogastric gavage for 7 consecutive days. Animals were humanely killed 24 hours after the last ovalbumin and drug exposure. Lung histopathologic findings were evaluated using light and electron microscopy. RESULTS: As evaluated in the control, placebo, dexamethasone, and glycyrrhizin groups, respectively, the mean (SD) basement membrane thickness was 306.34 (36.91), 657.52 (98.99), 405.13 (96.1), and 465.01 (121.48) nm; subepithelial smooth muscle thickness was 7.22 (1.37), 11.24 (1.85), 5.62 (1.15), and 7.76 (1.11) µm; epithelium thickness was 19.48 (1.22), 41.62 (5.49), 22.59 (3.18), and 25.54 (4.68) µm; number of mast cells was 1.34 (0.19), 3.62 (0.5), 2.06 (0.77), and 2.77 (0.23)/16,400 µm(2); and number of goblet cells was 0.32 (0.1), 4.92 (0.82), 0.66 (0.06), and 0.98 (0.15)/100 µm. Evaluation of lung histopathologic features demonstrated that the chronic asthma model of mice was successfully established, with significantly higher numbers of goblet and mast cells and increased thickness of epithelium, basement membrane, and subepithelial smooth muscle layers (P < 0.001 for all) in the asthma group compared with in the control group. The number of goblet (P < 0.001) and mast (P < 0.02) cells and the thickness of basement membrane (P < 0.001), subepithelial smooth muscle layers (P ≤ 0.001), and epithelium of the lung (P < 0.001) were found to be significantly lower in the glycyrrhizin group compared with in the placebo group. When the glycyrrhizin and dexamethasone groups were compared, there was no statistically significant difference between the 2 groups in the histopathologic parameters, including thickness of basement membrane (P = 0.514), subepithelial smooth muscle (P = 0.054), and epithelium (P = 1.0) and number of mast (P = 0.075) and goblet (P = 0.988) cells. CONCLUSIONS: The results of this study suggest that the group receiving glycyrrhizin had amelioration of all established chronic histopathologic changes of lung in the mouse model of asthma. Further studies are needed to evaluate the efficacy of glycyrrhizin in the management of asthma.

The effect of melatonin on experimentally-induced myringosclerosis in rats.

OBJECTIVES: This study determined the preventive effect of melatonin on the occurrence of experimentally-induced myringosclerosis of the tympanic membrane (TM). MATERIALS AND METHODS: Twenty Wistar albino-type rats weighing approximately 300 g each were randomly separated into two groups and myringotomized on the left TMs: group 1 rats (n=6) received intraperitoneal melatonin injections 10 mg/kg/day whereas group 2 rats (n=12) were treated with physiological serum only. The remaining two rats were served as the control group for histological comparison and standardization. After 15 days of treatment, myringotomized membranes were examined by otomicroscopy and harvested for histopathological evaluation. The functional effect of myringosclerotic plaques in the TMs of the two groups were compared with tympanometric measurements. RESULTS: Tympanic membranes in group 2 revealed extensive myringosclerotic plaques, on the other hand, TMs in group 1 showed faint or no existence of myringosclerosis. The mean magnitude of the maximum admittance from group 2 measured by tympanometry reduced to about 40% of the values obtained from group 1 (Z=-2,067, p=0.041). The mean magnitude of the maximum admittance from melatonin group was very close to the mean tympanometric value of non-myringotomized Wistar albino rats, demonstrating a functional outcome. CONCLUSION: The occurrence of myringosclerosis following experimental myringotomy can be hindered by systemic melatonin treatment.

Effects of Ginkgo biloba on airway histology in a mouse model of chronic asthma.

Platelet-activating factor (PAF) is an inflammatory mediator involved in the pathophysiology of asthma, suggesting a therapy antagonizing its effects may play a role in the disease treatment. The aim of the study was to determine the effects of Ginkgo biloba, a PAF antagonist, on lung histology. Thirty-five BALB/c mice were divided into five groups; A, B, C, D, and the control. All mice except controls were sensitized and challenged with ovalbumin. Mice in group A (placebo) received saline; group B received G. biloba, 100 mg/kg; group C received G. biloba, 150 mg/kg; and group D received dexamethasone, 1 mg/kg via orogastric gavage for 7 consecutive days. Chronic structural changes and airway remodeling were evaluated by using light and electron microscopy in all groups. Evaluation of lung histology indicated that the number of goblet cells, mast cells, thicknesses of epithelium, and basement membrane were significantly improved in groups B and C when compared with group A. There was no statistically significant difference in thicknesses of subepithelial smooth muscle between groups A, B, and C. When doses of G. biloba were compared with each other, only the number of goblet cells was significantly lower in group C than in group B. When G. biloba and dexamethasone groups were compared with each other, thicknesses of basement membrane and subepithelial smooth muscle were found to be lower in group D than in groups B and C. G. biloba alleviates all established chronic histological changes of lung except smooth muscle thickness in a mouse model of asthma.

Efficacy of sulphasalazine on lung histopathology in a murine model of chronic asthma.

Sulphasalazine is a specific inhibitor of nuclear factor kappa B (NF-kappa B) which plays a key role in asthma. To determine the impact of sulphasalazine in the treatment of chronic asthma, BALB/c mice were sensitized and challenged with ovalbumin. Mice with experimentally induced asthma in group I received saline, group II sulphasalazine 200 mg/kg, group III sulphasalazine 300 mg/kg, and group IV dexamethasone 1 mg/kg intraperitoneally once a day in the last 7 days of the challenge period. Histological findings of the airways were evaluated by light and electron microscopies. Dexamethasone and sulphasalazine in both doses significantly improved all airway histopathologic parameters of asthma except numbers of goblet cells. Both doses of sulphasalazine improved thicknesses of basement membrane better than dexamethasone. Dexamethasone reduced the number of mast cells better than sulphasalazine (200 mg/kg). Further studies are needed to evaluate the efficacy of sulphasalazine in the treatment of asthma.

Ginseng ameliorates chronic histopathologic changes in a murine model of asthma.

Currently, asthma therapies are effective in reducing inflammation but airway remodeling is poorly responsive to these agents. New therapeutic options that have fewer side effects and reverse chronic changes in the lungs are essential. This study aimed to determine the efficacy of oral administration of ginseng on lung histopathology in a murine model of chronic asthma. BALB/c mice were divided into four groups: control, placebo, ginseng, and dexamethasone. All mice except those in the control group were sensitized and challenged with ovalbumin. Then, mice in the ginseng group were given 2 gr/kg per day of ginseng and mice in the dexamethasone group received 1 mg/kg per day of dexamethasone via orogastic gavage once daily for 1 week. Lung histopathology was evaluated by using light and electron microscopy in all groups. All of the chronic changes of airways in the ginseng group were significantly ameliorated when compared with the placebo group. When compared with the dexamethasone group, the ginseng group had significantly lower numbers of mast cell count. Thicknesses of basement membrane, epithelium, and subepithelial smooth muscle were not statistically different between the ginseng and dexamethasone groups. Goblet cell numbers were much more reduced in the dexamethasone group. Ginseng is effective in resolving the established chronic histopathological changes of the lungs in the murine model of asthma.

The effects of selenium against cerebral ischemia-reperfusion injury in rats.

It is known that the brain tissue is extremely sensitive to ischemia-reperfusion (IR) injury and therefore, brain ischemia and consecutive reperfusion result in neural damage and apoptosis. The proinflammatory cytokines such as tumor necrosis factor alfa (TNF-alpha) and interleukin-1 beta (IL-1beta) are produced during neurological disorders including cerebral ischemia. On the other hand, nerve growth factor (NGF), which is essential for the differentiation, survival and functions of neuronal cells in the central nervous system, regulate neuronal development through cell survival and cell death signaling. In the present study, we aimed to investigate the effect of selenium (Se) on prefrontal cortex and hippocampal damage in rats subjected to cerebral IR injury. Selenium was injected intraperitoneally at the doses of 0.625 mg/(kg day) after induction of IR injury. Prefrontal cortex and hippocampal damage was examined by cresyl-violet staining. Apostain and caspase-3 immune staining were used to detect apoptosis. TNF-alpha, IL-1beta and NGF levels were also evaluated. Histopathological evaluation showed that treatment with selenium after ischemia significantly attenuated IR-induced neuronal death in prefrontal cortex and hippocampal CA1 regions of rats. Apoptotic cells stained with apostain and caspase-3 were significantly decreased in treatment group when compared with the IR group. Additionally, treatment with selenium decreased the TNF-alpha and IL-1beta levels and increased the NGF levels in prefrontal cortex and hippocampal tissue of animals subjected to IR. The present results suggest that selenium is potentially a beneficial agent in treating IR-induced brain injury in rats.

Saccharomyces boulardii prevents oral-poliovirus vaccine-induced IgA nephropathy in mice.

Immunoglobulin A nephropathy (IgAN) is associated with mucosal IgA defect. Probiotics regulate specific and innate immunity. We evaluated the effect of Saccharomyces boulardii on experimental IgAN in mice. Four groups of BALB/c mice (eight for each) were formed. Group 1 was immunized by oral poliovirus vaccine (OPV) at 0, 14, and 28 days. Group 2 was also given S. boulardii in addition to OPV. Group 3 was given only S. boulardii, whereas group 4 received no treatment. At week 6, after urine and serum samples were obtained for urinalysis and serum creatinine and IgA measurements, all animals were sacrificed to get their kidneys for histopathological evaluation. Urinalysis and serum creatinine levels were normal in all groups. Serum IgA level was increased only in group 1. Whereas group 1 had mesangial proliferation, histology was normal in the other groups. Predominant IgA deposition was universal in group 1, whereas it was either not present or minimal in other groups. Three mice in group 1 also had C3 deposition, which was absent in other groups. Electron microscopy revealed mesangial proliferation, matrix expansion, focal glomerular basement membrane thickening and electron-dense deposits in group 1 only, whereas the other groups were normal. In conclusion, enteral S. boulardii prevented OPV-induced IgAN in mice.