The possible effect of topically applied azithromycin and moxifloxacin on the alleviation of uveitis.

PURPOSE: To investigate the inhibitory effect of topically administered azithromycin (AZM), and moxifloxacin (MXF) against tumor necrosis factor-α (TNF-α) production in a rat model of endotoxin-induced uveitis (EIU). METHODS: Thirty-six Wistar albino rats were divided into 6 equal groups. Groups 1, 2 and 3 were determined as sham, control group for topical AZM application and control group for topical MXF application, respectively. Sterile saline, topical AZM 1.5%, and topical MXF 0.5% were instilled 5 times daily for totally 6 days on both eyes of the rats in Group 4, Group 5, and Group 6, before and after inducing EIU by intravitreal injections of lipopolysaccharide, respectively. At 24 h after intravitreal injections, aqueous humor was collected from both eyes of each rat for the assessment of TNF-α concentration. Also, density of nuclear factor kappa B (NF-κB) in ciliary body, and the number of cells infiltrating the posterior segment of EIU rat eyes was assessed in one eye of each rat. RESULTS: There was a significant reduction in mean aqueous humor concentration of TNF-α in EIU rats pretreated with topical AZM in comparison with those pretreated with sterile saline (139 ± 38.6 in Group 4 vs. 72 ± 12.6 in Group 5, p = 0.006). There was also a marked decrease in mean aqueous humor concentration of TNF-α in EIU rats pretreated with topical MXF (139 ± 38.6 in Group 4 vs.86.1 ± 35.5 in Group 6, p = 0.025). Also, evident suppressions were determined in mean density of NF-κB, and in mean number of cells in EIU rats pretreated either with topical AZM, or topical MXF. CONCLUSIONS: Topically applied AZM or MXF may be beneficial in the suppression of TNF-α production in aqueous humor.

Thymol regulates the Endothelin-1 at gene expression and protein synthesis levels in septic rats.

Sepsis is a serious systemic inflammatory response to infections. In this study, effects of thymol treatments on sepsis response were investigated. A total of 24 rats were randomly divided into 3 different treatment groups, namely as Control, Sepsis and Thymol. A sepsis model was created with a cecal ligation and perforation (CLP) in the sepsis group. For the treatment group, 100 mg/kg dose of thymol was administered via oral gavage and sepsis was established with a CLP after 1 h. All rats were sacrificed at 12 h post-opia. Blood and tissue samples were taken. ALT, AST, urea, creatinine and LDH were evaluated to assess the sepsis response in separated sera. Gene expression analysis was conducted for ET-1, TNF-α, IL-1 in lung, kidney and liver tissue samples. ET-1 and thymol interactions were determined by molecular docking studies. The ET-1, SOD, GSH-Px and MDA levels were determined by ELISA method. Genetic, biochemical and histopathological results were evaluated statistically. The pro-inflammatory cytokines and ET-1 gene expression revealed a significant decrease in the treatment groups, while there was an increase in septic groups. SOD, GSH-Px and MDA levels of rat tissues were significantly different in the thymol groups as compared to the sepsis groups (p < 0.05). Likewise, ET-1 levels were significantly reduced in the thymol groups. In terms of serum parameters, present findings were consistent with the literature. It was concluded based on present findings that thymol therapy may reduce sepsis-related morbidity, which would be beneficial in the early phase of the sepsis.

The importance of a disintegrin and metalloproteinase (ADAM)10 and ADAM17 in the pathogenesis of psoriasis.

BACKGROUND: Psoriasis is a chronic inflammatory skin disorder characterized by inflammation, hyperproliferation and neoangiogenesis. The disease pathogenesis has not been fully elucidated. The proteins, a disintegrin and metalloproteinase (ADAM)10 and ADAM17, are important proteases serving as regulators of inflammation. AIM: To determine the role of ADAM10 and ADAM17 in the pathogenesis of psoriasis through the comparison of their serum levels in patients with psoriasis and healthy controls (HCs). METHODS: In total, 179 participants (90 patients with psoriasis and 89 HCs) were enrolled in the study. Levels of ADAM10 and ADAM17 in serum were measured by ELISA for each participant from the patient and HC groups. The statistical data analysis was performed using SPSS (V19.0) and P < 0.05 was considered statistically significant. RESULTS: The mean values for serum ADAM10 and ADAM17 were, respectively, 3.1 ± 2.2 and 76.5 ± 31.1 in the psoriasis group and 8.6 ± 3.7 and 29.5 ± 22.4 in the HC group. A statistically significant difference between the patient and HC groups was detected for both ADAM10 and ADAM17 levels (P = 0.001). CONCLUSION: Considering the high levels of ADAM17 in the psoriasis group, ADAM17 protease might have a crucial role in the pathogenesis of psoriasis, while the low levels of ADAM10 might be attributable to its regulatory effect on keratinocyte differentiation and proliferation.

Association of abnormal coronary sinus reflux with coronary slow flow and importance of the Thebesian valve.

BACKGROUND: The relationship between coronary slow flow (CSF) and coronary sinus (CS) reflux has not been previously studied. This study aimed to investigate the relationship between CSF and CS reflux and Thebesian valve presence as well as the relationship between CS reflux and serum annexin-V and ICAM-1 levels. METHODS: In this case-control study, patients were divided into two groups: CSF (n = 13) and control (n = 7) groups. CS flow parameters and Thebesian valve presence were evaluated by cardiac magnetic resonance (CMR). Moreover, serum ICAM-1 and annexin-V levels were measured. RESULTS: Regurgitation volume and regurgitation fraction, indicators of reflux flow in CS, were higher in the CSF group than in the control group (p = 0.039 and p = 0.019). Fewer Thebesian valves were observed in the CSF group than in the control group (p = 0.022). Furthermore, a positive correlation was found between regurgitation volume and regurgitation fraction and serum annexin-V and ICAM-1 levels (r = 0.813, p < 0.001 and r = 0.996, p < 0.001; r = 0.817, p < 0.001 and r = 0.993, p < 0.001, respectively). CONCLUSIONS: This study revealed the significant relationship between CSF and reflux flow in CS. The fact that the patients in the CSF group have fewer Thebesian valves suggests the importance of the valve in preventing backward flow from the coronary vein. A positive correlation between serum ICAM-1 and annexin-V levels with regurgitation volume and regurgitation fraction indicates that after a certain threshold, CS reflux should be considered an abnormal condition.

Quercetin associated with dimethylsulfoxide has a curative effect on experimental colon anastomosis injury.

Purpose To examine the effects of quercetin on healing of experimental colon anastomosis injury in early and late period. Methods Eighty male Wistar-Albino rats were divided into 8 groups. For all groups, left colons of the rats were resected and for the rest end-to-end anastomosis was performed. Two of the groups for which the experiment protocol was ended on the 3rd and 7th day following the anastomosis were not administered with either quercetin or dimethylsulfoxide DMSO, whereas two other groups were administered with DMSO only, and four other groups were administered with quercetin dissolved in DMSO in doses of 20 and 100 mg/kg during the protocol. At the end of the study, anastomosis line was resected, histopathological evaluation was performed and bursting pressure, malondialdehyde, superoxide dismutase, catalase, and hydroxyproline levels were measured. Results Quercetin significantly increased hydroxyproline, superoxide dismutase, catalase levels, histopathological healing score, bursting pressure values and decreased malondialdehyde level in early period. It also significantly increased superoxide dismutase, catalase, and hydroxyproline levels and decreased malondialdehyde level in late period. Conclusion It was seen that quercetin speeds up the injury healing process and reveals an antioxidant effect, specifically in early period.

Ozone treatment for high-dose systemic Steroid-Induced retinal injury.

OBJECTIVE: To investigate the effect of high-dose systemic steroids on retinal tissues and the effectiveness of ozone (O3) therapy. METHODS: Twenty-four New Zealand white rabbits were divided into three groups of eight. Group 1 was accepted as the control group, Group 2 received intramuscular 20 mg/kg methylprednisolone acetate and Group 3 received 14 sessions of ozone treatment in addition to methylprednisolone acetate. The subjects were sacrificed on the 30th day. Retinal tissues were removed. Superoxide dismutase (SOD), catalase (CAT), malondialdehyde (MDA), total antioxidant status (TAS) and total oxidant status (TOS) levels were evaluated for tissue biochemistry and serum ischaemic modified albumin (IMA), interleukin-6 (IL-6) and tumour necrosis factor-α (TNF-α) levels were evaluated with the ELISA method. Haematoxylin-eosin staining and TUNEL evaluation for apoptosis were evaluated as histopathological methods. RESULTS: In the treatment group, antioxidant parameters of TAS, SOD and CAT were higher, oxidative and ischaemic parameters of MDA, TOS and IMA were lower, inflammatory parameters of IL-6 and TNF-α were lower, retinal thickness was better and apoptosis amount was lower. CONCLUSION: Apoptosis increases in retinal tissues due to high dose systemic steroid administration and the retina becomes thinner. With biochemical examination, oxidation parameters increased while antioxidant parameters decreased. Both histopathological and biochemical parameters improved significantly with ozone treatment.

Melatonin ameliorates sodium valproate-induced hepatotoxicity in rats.

Valproic acid (VPA) is a anticonvulsant and mood-stabilizing agent used to treat epilepsy in patients of all ages. However, it can cause hepatotoxicity with increased oxidative stress. Melatonin (MEL) is known as antioxidant and antiinflammatory agent. Therefore, the present study designed to investigate the probable protective role of melatonin against VPA-induced liver toxicity. For that purpose, 28 Wistar rats were randomly selected and divided into four groups, namely the Group C (vehicle), VPA (500 mg/kg/day VPA), MEL + VPA (10 mg/kg/day melatonin + 500 mg/kg/day VPA) and MEL (10 mg/kg/day melatonin). The agents were given by oral gavage for 14 days. Blood and liver tissue samples from all the rats were harvested on the 15th day of experiment. Biochemical analyses were conducted on the blood samples. The levels of malondialdehyde (MDA), superoxide dismutase (SOD), alpha glutathione S-transferases (α-GST), nuclear factor-κB (NF-κB), myeloperoxidase (MPO) and changes in gene expression were examined in the liver tissues. Also, liver histopathological analyses were conducted. VPA administration significantly increased the levels of α-GST, MDA, NF-κB and of IL-1ß, TNF-α gene expression in the liver compared to Group C. Moreover, vacuolization, hydropic degeneration, inflammatory cell infiltration, and sinusoidal congestion were commonly detected in the VPA-treated group along with the highest apoptotic index (TUNEL staining) values. Melatonin administration was revealed to exhibit powerful protective properties at cellular, inflammatory and oxidative level activities against VPA-induced liver toxicity. Therefore, melatonin administration may be used as an adjuvant therapy against to VPA-induced liver toxicity.

The hepatoprotective effect of Aloe vera on ischemia-reperfusion injury in rats.

OBJECTIVE: Aloe vera is known for its antioxidant properties. In this experimental study, we aimed to investigate the efficacy of Aloe vera in ischemia-reperfusion (I/R) liver injury in rats. METHODS: Male Wistar Albino rats were divided into three groups, where the sham group (n=7) underwent no medication or surgical procedures, the I/R group (n=7) was the control group that received 45 minutes of applied abdominal aorta ischemia and rats were sacrificed 24 hours after reperfusion, and the I/R+AV group (n=7) was the treatment group that was given Aloe vera (30 mg/kg) every day followed by gastric lavage for a month before applying ischemia and performing sacrifice as in the previous group. Before sacrifice, all the liver tissues were removed. Tissues were examined for histopathological investigation, iNOS immunoreactivity and tissue biochemistry, malondialdehyde (MDA), catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px) activities. RESULTS: The SOD, CAT, and GSH-Px levels of the I/R+AV group were not significantly different from the sham group (p>0.05) but were significantly higher when compared to the I/R group. MDA levels of liver tissues were significantly lower (p<0.05) in the I/R+AV group as compared to the I/R group. Disrupted hepatic cords, sinusoidal dilatation, hemorrhage, cytoplasmic vacuolization of hepatocytes, and intensive iNOS immunoreactivity were detected in the I/R group. Decreased histopathological change score and iNOS immunoreactivity score were noticed in the I/R+AV group as compared to the I/R group. CONCLUSION: It was found that Aloe vera showed a hepatoprotective effect against I/R injury. Further research is required to determine the effective dose, administration method, and effects of Aloe vera for liver transplantation.

Hyperbaric oxygen treatment ameliorates gentamicin-induced nephrotoxicity and expression of kidney injury molecule 1 in the rat model.

In recent years hyperbaric oxygen (HBO2) therapy has been considered as an effective method for the treatment of gentamicin (GM)-induced renal toxicity. However, the findings related to the use of HBO2 for GM toxicity are limited and contradictory. The aim of this study is to investigate the protective role of HBO2 on GM-induced nephrotoxicity. For this purpose, Wistar albino rats (n=28) were randomly divided into four equal groups: C, HBO2, GM and GM+HBO2. GM (100 mg/kg, ip) and HBO2 were applied over seven days. On the eighth day blood and kidney tissue samples were harvested. The albumin, creatinine, and urea levels were determined from serum samples. Superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) activities, malondialdehyde (MDA), total antioxidant status (TAS) and total oxidant status (TOS) values were analyzed spectrophotometrically. The relative expression level of TNF-α, IL-1ß and Kim-1 gene were determined by qRT-PCR assays; histopathologic investigation was completed in kidney tissue samples. Serum urea, albumin and creatinine levels significantly increased in the GM group compared to the GM+HBO2 group. For antioxidant parameters the GM+HBO2 group was not statistically different from the C group but was significantly different compared with the GM group. TNF-α, IL-1ß and Kim-1 gene expression levels in the GM group were statistically increased compared to the GM+HBO2 group (p=0.015, p=0.024, p=0.004) respectively. Severe tubular necrosis, epithelial desquamation and mild peritubular hemorrhage were observed in the GM-administrated group, while HBO2 exposure ameliorated these alterations. In conclusion, HBO2 exposure may be defined as a potential method for the prevention of GM-induced renal toxicity.

Protective effect of gel form of gastric gavage applicated aloe vera on ischemia reperfusion injury in renal and lung tissue.

The aloe vera plant has become increasingly popular in recent years. This study aimed to research the effect of aloe vera to prevent renal and lung tissue damage in an experimental ischemia-reperfusion (I/R) injury model. The study included 21 male Wistar Albino rats, which were categorized into control group, n = 7 (no procedures), Sham group n = 7 (I/R); and aloe vera therapy group, n = 7 (aloe vera and I/R). Superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), and malondialdehyde (MDA) were evaluated from lung and kidney tissues for biochemical investigations. As histopathological, hematoxylin and eosin and anti-iNOS were also examined. In biochemical investigations, SOD, CAT, and GPx levels of the Sham group were found to be lower compared with the other groups (P < 0.05). The aloe vera therapy group was not statistically different from control groups but significantly different compared with the Sham group. In the same way, the MDA levels of kidney and lung tissues were statistically significant in the aloe vera therapy group, compared to the Sham group. In the Sham group, the peribronchial and perialveolar edema were observed in lung parenchyma. Also, excess interstitial hemorrhage, leukocyte infiltration, and alveolar wall thickening were identified in ischemic groups. The histopathological changes were much lighter than in the aloe vera therapy group. In renal tissues, excess epithelial cell deterioration, tubular desqumination, and glomerular atrophy were observed in the Sham group. The histopathological changes were markedly reduced in the aloe vera therapy  group. In the kidney and lung tissue, the level of iNOS activity in the Sham group was significantly higher than in the control and aloe vera therapy group. This study indicated that aloe vera is protective against oxidative damage formed by I/R in distant organs like the lungs and kidneys.

The effects of apomorphine on paracetamol-induced hepatotoxicity in rats.

It is becoming progressively more understandable that overdose of paracetamol in both humans and animals causes severe hepatotoxicity. Apomorphine is known as a neuroprotective agent. Due to the protective effect,  apomorphine had been tested in experimental studies on different models. Findings obtained through series of expriments suggested that apomorphine may also be useful in liver toxicity. The aim of this study is to investigate the relationship among the hepatoprotective mechanism of apomorphine and to determine the possible role of apomorphine on paracetamol-induced hepatotoxicity in rats. 30 Sprague Dawley rats (adult male) were distributed into 5 groups. Group 1 was the control group and did not receive any medication. Group 2 received only paracetamol 2 g/kg by intragastric gavage to induce hepatotoxicity. Groups 3 and 4 were given apomorphine 1 mg/kg and 2 mg/kg by intraperitoneal injection, respectively. Groups 3 and 4 were given 2g/kg  of Paracetamol. In Group 5, rats were treated with 2 mg/kg of apomorphine. Drug-treated rats were given food for the next 24 h until they were sacrified. Moreover, we also performed AST, ALT measurements in serum, MDA and SOD levels in liver tissues and histopathological analysis of the liver in all groups. Apomorphine had positive effects on both liver enzymes, oxidative stress markers and histopathological results in paracetamol-induced hepatotoxicity. Additionally, apomorphine at 2 mg/kg dose was significantly more protective as compared to 1 mg/kg as evidenced by the histopathological examination results. It was thought that apomorphine was found hepatoprotective on paracetamol-induced hepatotoxicity, especially at higher doses such as 2 mg/kg.

The Axon Protective Effects of Syringic Acid on Ischemia/Reperfusion Injury in a Rat Sciatic Nerve Model.

AIM: In the relevant literature, there is no experimental study that investigated the axon protective effects of syringic acid- a polyphenol compound- with an anti-oxidant capacity on ischemia/reperfusion injury. MATERIAL AND METHODS: The rats were randomly divided into four groups: Control group (no medication or surgical procedure), Sham group, Syringic acid group, and Methyprednisolone (MP) Group. Ischemia was achieved by abdominal aorta clamping and all animals were sacrificed 24 hours after ischemia. Harvested sciatic nerve segments were investigated histopathologically and for tissue biochemistry. RESULTS: Ischemic fiber degeneration scores were found significantly lower in syringic acid and MP groups than sham group. Additionally, apoptosis-related cysteine peptidase caspase-3 immunostaining scores were lower in syringic acid and MP groups. Biochemically, superoxide dismutase and nuclear respiratory factor 1 values were significantly higher in syringic acid group compared to those of control and sham groups while malondialdehyde levels were significantly lower in the syringic acid group. CONCLUSION: Syringic acid reduces oxidative stress and axonal degeneration in rat sciatic nerve after ischemia/reperfusion injury. Therefore, syringic acid may play a role in the treatment of peripheral nerve injuries due to ischemia/reperfusion.

Effects of Aloe Vera on Spinal Cord Ischemia-Reperfusion Injury of Rats.

AIM: The purpose of this study was to evaluate the possible protective/therapeutic effects of aloe vera (AV) on ischemia-reperfusion injury (I/R) of spinal cord in rats. MATERIALS AND METHODS: A total of 28 Wistar Albino rats were divided into four random groups of equal number (n = 7). Group I (control) had no medication or surgery; Group II underwent spinal cord ischemia and was given no medication; Group III was administered AV by gastric gavage for 30 days as pre-treatment; Group IV was administered single dose intraperitoneal methylprednisolone (MP) after the ischemia. Nuclear respiratory factor-1 (NRF1), malondialdehyde (MDA) and superoxide dismutase (SOD) levels were evaluated. Tissue samples were examined histopathologically and neuronal nitric oxide synthase (nNOS) and nuclear factor-kappa B (NF-κB) protein expressions were assessed by immunohistochemical staining. RESULTS: NRF1 and SOD levels of ischemia group were found to be lower compared to the other groups. MDA levels significantly increased after I/R. Treatment with AV and MP resulted in reduced MDA levels and also alleviated hemorrhage, edema, inflammatory cell migration and neurons were partially protected from ischemic injury. When AV treatment was compared with MP, there was no statistical difference between them in terms of reduction of neuronal damage. I/R injury increased NF-κB and nNOS expressions. AV and MP treatments decreased NF-κB and nNOS expressions. CONCLUSIONS: It was observed that aloe vera attenuated neuronal damage histopathologically and biochemically as pretreatment. Further studies may provide more evidence to determine the additional role of aloe vera in spinal cord ischemia reperfusion injury.

Increased Levels of Serum Ischemia Modified Albumin in Patients with Ankylosing Spondylitis.

BACKGROUND: The aim of the study was to investigate oxidant/antioxidant status by determining serum ischemia-modified albumin (IMA) levels with oxidative/antioxidant parameters in patients with ankylosing spondylitis (AS) compared to the controls. METHODS: The serum concentrations of IMA, IMA/albumin ratio (IMAR), malondialdehyde (MDA), total oxidant status (TOS), oxidative stress index (OSI), superoxide dismutase (SOD), glutathione peroxidase (GPx), and total antioxidant capacity (TAC) were measured in 40 AS patients and 35 healthy controls. RESULTS: Mean serum IMA, IMAR, MDA, TOS, and OSI levels were increased in patients with AS when compared to the control group (p < 0.05 for all). Serum levels of SOD and GPx were significantly lower in the patient group than in the healthy subjects (p < 0.001 for both). Serum TAC levels were decreased in patients with AS compared to the controls but the statistical difference was not significant. Serum IMA levels were found to be positively correlated with BASDAI, BASFI, BASMI, and ASDAS-CRP (r = 0.356, r = 0.370, r = 0.412, r = 0.353, respectively, and p < 0.05 for all). IMAR values showed significant correlations with BASFI, BASMI, and ASDAS-CRP (r = 0.351, p = 0.026; r = 0.400, p = 0.010; and r = 0.379, p = 0.016, respectively). CONCLUSIONS: Depletion in antioxidant systems and overproduction of free radicals leading to formation of the oxidative stress may play a role in the development of AS. Increased levels of IMA might provide important contributions to the underlying oxidative stress in AS.

The effect of aloe vera on ischemia--Reperfusion injury of sciatic nerve in rats.

PURPOSE: Aloe vera is compound which has strong antioxidant and anti-inflammatory effects. We investigated the neuroprotective role of aloe vera treatment in rats with experimental sciatic nerve ischemia/reperfusion injury. METHODS: Twenty-eight male Wistar Albino rats were divided equally into 4 groups. Groups; Control group (no surgical procedure or medication), sciatic nerve ischemia/reperfusion group, sciatic nerve ischemia/reperfusion+aloe vera group and sciatic nerve ischemia/reperfusion+methylprednisolone group. Ischemia was performed by clamping the infrarenal abdominal aorta. 24 hours after ischemia, all animals were sacrificed. Sciatic nerve tissues were also examined histopathologically and biochemically. RESULTS: Ischemic fiber degeneration significantly decreased in the pre-treated with aloe vera and treated with methylprednisolone groups, especially in the pre-treated with aloe vera group, compared to the sciatic nerve ischemia/reperfusion group (p<0.05). A significant decrease in MDA, an increase in NRF1 level and SOD activity were observed in the groups which obtained from the AV and MP groups when compared to the sciatic nerve ischemia/reperfusion group. When all results were analysed it was seen that the aloe vera group was not statistically different compared to the MP group (p>0.05). CONCLUSIONS: Aloe vera is effective neuroprotective against sciatic nerve ischemia/reperfusion injury via antioxidant and anti-inflammatory properties. Also aloe vera was found to be as effective as MP.

The Neuroprotective Effect of Kefir on Spinal Cord Ischemia/Reperfusion Injury in Rats.

OBJECTIVE: The main causes of spinal cord ischemia are a variety of vascular pathologies causing acute arterial occlusions. We investigated neuroprotective effects of kefir on spinal cord ischemia injury in rats. METHODS: Rats were divided into three groups : 1) sham operated control rats; 2) spinal cord ischemia group fed on a standard diet without kefir pretreatment; and 3) spinal cord ischemia group fed on a standard diet plus kefir. Spinal cord ischemia was performed by the infrarenal aorta cross-clamping model. The spinal cord was removed after the procedure. The biochemical and histopathological changes were observed within the samples. Functional assessment was performed for neurological deficit scores. RESULTS: The kefir group was compared with the ischemia group, a significant decrease in malondialdehyde levels was observed (p<0.05). Catalase and superoxide dismutase levels of the kefir group were significantly higher than ischemia group (p<0.05). In histopathological samples, the kefir group is compared with ischemia group, there was a significant decrease in numbers of dead and degenerated neurons (p<0.05). In immunohistochemical staining, hipoxia-inducible factor-1α and caspase 3 immunopositive neurons were significantly decreased in kefir group compared with ischemia group (p<0.05). The neurological deficit scores of kefir group were significantly higher than ischemia group at 24 h (p<0.05). CONCLUSION: Our study revealed that kefir pretreatment in spinal cord ischemia/reperfusion reduced oxidative stress and neuronal degeneration as a neuroprotective agent. Ultrastructural studies are required in order for kefir to be developed as a promising therapeutic agent to be utilized for human spinal cord ischemia in the future.

The Effect of Coumaric Acid on Ischemia-Reperfusion Injury of Sciatic Nerve in Rats.

The aim of the study was to determine the effect of coumaric acid on sciatic nerve ischemia/reperfusion (SNI) injury in rats. The rats were randomly divided into four groups: control group (no medication or surgical procedure), SNI group, SNI + coumaric acid (CA) group, and SNI + methylprednisolone (MP) group. Ischemia was achieved by abdominal aorta clamping, and all animals were sacrificed 24 h after ischemia. Harvested sciatic nerve segments were investigated histopathologically and for tissue biochemistry. A significant decrease in MDA, an increase in NRF1 levels, and increase in SOD activity were observed in the groups which received coumaric acid and methylprednisolone when compared to the corresponding untreated group (p < 0.05). Ischemic fiber degeneration significantly reduced in the SNI + CA and SNI + MP groups, especially in the SNI + MP group, compared to the SNI group (p < 0.05). Beta amyloid protein expressions were significantly decreased in the SNI + CA group compared to the SNI group (p < 0.05). Our study revealed that coumaric acid treatment after ischemia/reperfusion in rat sciatic nerves reduced oxidative stress and axonal degeneration. Therefore, coumaric acid may play a role in the treatment of peripheral nerve injuries due to ischemia/reperfusion.

The Neuroprotective Effect of Coumaric Acid on Spinal Cord Ischemia/Reperfusion Injury in Rats.

The main causes of spinal cord ischemia are a variety of vascular pathologies causing acute arterial occlusions. We investigated neuroprotective effects of coumaric acid on spinal cord ischemia injury in rats. Rats were divided randomly into four groups of eight animals as follows: control, ischemia, ischemia + coumaric acid, and ischemia + methylprednisolone. In the control group, only a laparotomy was performed. In all other groups, the spinal cord ischemia was performed by the infrarenal aorta cross-clamping model. Levels of malondialdehyde and nuclear respiratory factor 1 were analyzed, as were the activity of superoxide dismutase. Histopathological and immunohistochemical evaluations were performed. Neurological evaluation was performed with the Tarlov scoring system. The ischemia + coumaric acid group was compared with the ischemia group, and a significant decrease in malondialdehyde and levels was observed. Nuclear respiratory factor 1 level and superoxide dismutase activity of the ischemia + coumaric acid group were significantly higher than in the ischemia group. In histopathological samples, the ischemia + coumaric acid group is compared with the ischemia group, and there was a significant increase in numbers of normal neurons. In immunohistochemical staining, hypoxia-inducible factor-1α and NF-kappa B immunopositive neurons were significantly decreased in the ischemia + coumaric acid group compared with that in the ischemia group. The neurological deficit scores of the ischemia + coumaric acid group were significantly higher than the ischemia group at 24 h. Our results revealed for the first time that coumaric acid exhibits meaningful neuroprotective activity following ischemia-reperfusion injury of the spinal cord.

The Neuroprotective Effect of Syringic Acid on Spinal Cord Ischemia/Reperfusion Injury in Rats.

Acute arterial occlusions via different vascular pathologies are the main causes of spinal cord ischemia. We investigated neuroprotective effects of syringic acid on spinal cord ischemia injury in rats. Rats were divided into four groups: (I) sham-operated control rats, (II) spinal cord ischemia group, (III) spinal cord ischemia group performed syringic acid, and (IV) spinal cord ischemia group performed methylprednisolone intraperitoneally. Spinal cord ischemia was performed by the infrarenal aorta cross-clamping model. The spinal cord was removed after the procedure. The biochemical and histopathological changes were observed within the samples. Functional assessment was performed for neurological deficit scores. A significant decrease was seen in malondialdehyde levels in group III as compared to group II (P < 0.05). Besides these, nuclear respiratory factor-1 and superoxide dismutase activity of group III were significantly higher than group II (P < 0.05). In histopathological samples, when group III was compared with group II, there was a significant decrease in numbers of apoptotic neurons (P < 0.05). In immunohistochemical staining, BECN1 and caspase-3-immunopositive neurons were significantly decreased in group III compared with group II (P < 0.05). The neurological deficit scores of group III were significantly higher than group II at twenty-fourth hour of ischemia (P < 0.05). Our study revealed that syringic acid pretreatment in spinal cord ischemia/reperfusion reduced oxidative stress and neuronal degeneration as a neuroprotective agent. Ultrastructural studies are required for syringic acid to be developed as a promising therapeutic agent to be utilized for human spinal cord ischemia in the future.