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.

Topical Application of Cyclosporine Reduces Epineurial Fibrosis: Gross Postsurgical, Histopathological and Ultrastructural Analysis in a Rat Sciatic Nerve Model.

AIM: To investigate the antiscarring potential of topical cyclosporine on rat sciatic nerves. MATERIAL AND METHODS: Both sciatic nerves were exposed in 24 adult male albino Wistar rats, and an abrasion injury was made on the biceps femoris close to the sciatic nerve. Cotton pads soaked with cyclosporine (5 mg/mL) and saline (0.9% NaCl) were placed around the nerves for 10 minutes in the experimental group and control group, respectively. All rats were sacrificed 8 weeks later and the sciatic nerves were examined. Epineural adhesions were assessed using light and electron microcopy. Quantitative histologic parameters, epineurial thickness, and scar density were evaluated in the histologic investigation. RESULTS: Significantly fewer epineurial adhesions were observed in the cyclosporine group in the postsurgical assessment, and the histopathologic and ultrastructural examination of the nerve segments than in the controls. The cyclosporine-treated animanls had a statistically significant reduction in the density and quantity of epineurial scarring compared with the controls. CONCLUSION: Topical cyclosporine effectively reduced epineurial scar formation on rat sciatic nerves.

The effects of tibolone on the human primary glioblastoma multiforme cell culture and the rat C6 glioma model.

OBJECTIVES: In the light of recent advances in tumor biology and genetics, we hypothesized that tibolone, an estrogen receptor agonist, may have antiproliferative effects on primary human glioblastoma cells and rat C6 malignant glioma cell lines. We thought that tibolone should exert its antiproliferative effects by augmenting glial cell differentiation through the naive, nonhypermethylated estrogen receptors in the glioma cells. METHODS: Human primary glioblastoma multiforme (GBM) cells were acquired perioperatively from ten patients aged between 45 and 69 years, diagnosed clinically and radiologically with GBM. The diagnosis was confirmed using immunohistochemical assays. Human GBM and rat C6 malignant glioma cells were cultivated in vitro to obtain monolayer cell cultures. Tibolone was then applied to these cultures in wells, each containing 500,000 tumor cells. RESULTS: Tibolone significantly decreased the number of human GBM cells at the concentrations of 10 and 100 mg/ml. For tibolone, a strong dose-dependent correlation in tumor inhibition was found (p=0.001). This antiproliferative effect of tibolone in human GBM cells was not observed in rat C6 malignant glioma cells. Tibolone demonstrated differential effects on human GBM and rat C6 glioma cells. DISCUSSION: In vitro antiproliferative effects of tibolone on human GBM need to be investigated further in in vivo works.

Effect of magnesium, MK-801 and combination of magnesium and MK-801 on blood-brain barrier permeability and brain edema after experimental traumatic diffuse brain injury.

OBJECTIVE: Glutamate antagonists are very attractive drugs in laboratory works to protect neural tissue against ischemia. In this work, the effects of magnesium, MK-801 and combination of magnesium and MK-801 on blood-brain barrier (BBB) and brain edema after experimentally induced traumatic brain injury are evaluated. METHODS: A standard closed head injury was induced on the rats by a controlled impact device using a 450-g free falling mass from a height of 2 m onto a metallic disc fixed to the intact skull. One of the following was injected to animals intraperitoneally 30 minutes after injury: saline, magnesium, MK-801 and magnesium plus MK-801. To quantify the brain edema, the specific gravity of the brain tissue was determined. To demonstrate the alteration of the BBB permeability, Evans blue dye was used as a tracer. RESULTS: In all treatment groups, the specific gravity of brain tissue values was significantly higher compared with the control group. Evans blue dye content in the brain tissue was significantly reduced in all three treatment groups with respect to the control group. There was no significant difference of effect between the groups of magnesium alone and MK-801 alone when compared with each other and when compared with their combination. CONCLUSION: The present data demonstrate that treatment with magnesium, MK-801 and combination of magnesium and MK-801 can reduce formation of brain edema and can help restore BBB permeability after experimental diffuse brain injury.