Effect of Taxifolin on Ischemia/Reperfusion-Induced Oxidative Injury of Sciatic Nerve in Rats.

BACKGROUND: Ischemia is a condition in which blood flow to tissues is decreased or entirely stopped for various reasons. The reperfusion process exacerbates damage caused by ischemia in the organs and tissues. Reactive oxygen species (ROS) are mainly responsible for ischemia-reperfusion (IR) damage. ROS increase results in lipid peroxidation (LPO) and oxidative stress. In the literature, taxifolin reportedly suppresses ROS production. This study aimed to determine the effect of taxifolin, which is a flavonoid, on IR injury of the sciatic nerve in rats. METHODS: This study divided 30 albino Wistar rats into 3 groups: IR without medication (IR) group, taxifolin applied IR (TAX+IR) group, and only dissection made to the sciatic nerve sham group (SHAM). Sciatic nerve injury was induced by applying 2 hours of ischemia and 3 hours of reperfusion to the abdominal aorta and iliolumbar arteries. Biochemical and histopathologic investigations then were performed on sciatic nerve tissues. Malondialdehyde, total glutathione, glutathione reductase, and glutathione peroxidase were analyzed as oxidative stress markers, and tumor necrosis factor-α and interleukin-1ß levels were evaluated as inflammatory stress markers in biochemical tests. RESULTS: The IR group has statistically significantly high oxidant and cytokine levels and low antioxidant levels compared with the TAX+IR group. Taxifolin treatment was also shown to cause significant histopathologic improvement. CONCLUSIONS: We suggest that taxifolin may be effective in preventing IR injury of the sciatic nerve.

The Effect of Lutein on Ischemia-reperfusion-induced Vasculitic Neuropathic Pain and Neuropathy in Rats.

BACKGROUND/AIM: Neuropathic pain and neuropathy is commonly seen after ischemia-reperfusion injuries. Our aim was to evaluate the effect of lutein on ischemia-reperfusion (I/R)-induced vasculitic neuropathic pain and neuropathy in rats. MATERIALS AND METHODS: An hour before anesthesia, 6 Albino Wistar male rats with I/R were orally administered with 1 mg/kg lutein (LIR group). Two groups of 6 such rats who underwent surgery were provided with 0.5 ml distilled water (as solvent) either via oral administration (SIR group) or by gavage (sham group or SG). One hour following the administration, the later femoral arteries of the LIR and SIR rats were closed using a sterile silk thread and ischemia was induced in the sciatic nerve for 4 h, followed by reperfusion for 24 h. The femoral artery of the SG group was not closed with suture. Next, 1 mg/kg lutein was re-administered only to the LIR group for 1 h, followed by measurement of the paw pain thresholds by the Basile Algesimeter. The levels of malondialdehyde (MDA), total glutathione (tGSH), nuclear factor-kB (NF-κB), and tumor necrosis factor-alpha (TNF-α) in the sciatic nerve tissues were measured, and the tissues were histopathologically examined. RESULTS: We found that the MDA, NF-κB, and TNF-α levels were higher and the tGSH level was lower in the SIR group relative to those in the LIR group, and the differences were statistically significant. Significant histopathological damage was noted in the SIR group, whereas the LIR group demonstrated protection from oxidative damage. CONCLUSION: Lutein is potentially useful in the treatment of I/R-related neuropathy and neuropathic pain.

The Effect of Rutin on Experimental Traumatic Brain Injury and Edema in Rats.

BACKGROUND/AIM: The aim of the study was to evaluate the effect of rutin, which is a vitamin P1 flavonoid with anti-inflammatory and anti-edema effects, on traumatic brain injury (TBI) and edema in rats. MATERIALS AND METHODS: Rats were divided into 3 groups as sham group without brain trauma (SG), brain trauma without medication (BT) group and Rutin treated brain trauma (RBT) group. Fifty mg/kg rutin was administered to the RBT group once a day for three days. On the fourth day, rats were sacrificed. Extracted brain tissues were examined biochemically and histopathologically. RESULTS: We found that the levels of malondialdehyde, nuclear factor-kappa B and tumor necrosis factor-alpha decreased, and those of total glutathione increased significantly. Furthermore, rutin administration reduced pyramidal neuron degeneration and poly-morpho-nuclear-leucocyte accumulation due to trauma in brain tissue, while eliminating edema. CONCLUSION: Rutin might be effective in the treatment of TBI and TBI-related brain edema.

Effects of pycnogenol on ischemia/reperfusion-induced inflammatory and oxidative brain injury in rats.

BACKGROUND: Ischemia/reperfusion (I/R) injury results from the onset of re-circulation following a perfusion deterioration period in the tissues, resulting in more damage than that caused by perfusion deterioration. This study aimed to determine the effects of pycnogenol on I/R injury in rat brain tissues. METHODS: Eighteen albino Wistar rats were divided into three groups: I/R injury (IR, n = 6) group; I/R injury + pycnogenol (IR + P, n = 6) group; and sham group (SG, n = 6). After 30 min of transient ischemia, 24 h of reperfusion was achieved in the IR and IR + P groups. Surgical dissection, except for transient ischemia, was performed in SG. Next, histopathological and biochemical investigations were performed on brain tissues. Malondialdehyde (MDA), reduced glutathione (GSH), and glutathione peroxidase (GPO) were analyzed as oxidative stress markers; IL-1ß and TNF-α were analyzed as inflammatory stress markers in biochemical tests. RESULTS: Histopathological examination revealed normal morphology in SG and diffuse cortex damage with edema, vasopathology, and inflammatory cell infiltration in the IR group. The IR + P group showed less cortex damage, edema, and vasopathology than the IR group. The MDA, IL-1ß, and TNF-α levels were significantly higher in the IR group than those in the SG group. The values of same markers for the IR + P group were significantly lower than the IR group. The GSH and GPO levels were significantly decreased with IR damage, but PYC treatment showed significant improvement in the levels. CONCLUSION: This study showed that the administration of pycnogenol ameliorated brain damage after I/R injury by reducing oxidative and inflammatory damage in the rat brain.

Morphometric Assesment of the External Anatomy of Fourth Ventricle and Dorsal Brainstem in Fresh Cadavers.

AIM: To investigate the external anatomy of the fourth ventricle and dorsal brainstem using morphometric data, which could be useful for preoperative surgical planning. MATERIAL AND METHODS: Between January 2017 and December 2017, 42 fresh adult cadavers were investigated for the measurements of the cadaver brainstems and fourth ventricle, and they were recorded by photography. Measurements were evaluated according to body mass indexes (BMIs) of the patients. We also investigate the visualization of facial colliculus and stria medullaris on brainstem. RESULTS: A total of 42 fresh cadavers with a mean age of 45.38 ± 16.41 years old were included in this research. We found no statistically significant difference between measurements and BMIs. Facial colliculus was visualized in 92.9% (n=39), but it could not visualized in 7.1% (n=3) of the subjects. When the right side of the stria medullaris was examined, one bundle was seen in 59.5% (n=25) of the subjects, two bundles were seen in 31% (n=13) of the subjects, and 3 bundles were seen in 9.5% (n=4) of the subjects. When the left side of the stria medullaris was examined, one bundle was seen in 57.1% (n=24) of the subjects, two bundles were seen in 33.3% (n=14) of the subjects, and three bundles were seen in 9.5% (n=4) of the subjects. CONCLUSION: Knowledge of the normal morphometry of the dorsal brainstem as it has been reported in this study will help one to assess distortions in any preoperative imaging studies and surgical planning.

Assessment of the neuroprotective effects of the acetylcholinesterase inhibitor huperzine A in an experimental spinal cord trauma model.

BACKGROUND: Spinal cord injury is nowadays still a challenging disease, and a treatment option aimed at the primary site of injury does not currently exist. Therefore, the management of acute spinal cord injury has recently focused on the reasons behind the aggravation of the initial insult through secondary mechanisms, and the search for pharmacological treatment protocols is generally aimed at reducing and minimizing the neural injury and neurological sequela. The secondary spinal cord injury usually develops following a primary lesion induced by spinal cord contusion and the emergence of apoptotic cells has been found to play an important role in the development of secondary injury. We propose that huperzine A may induce a significant reduction in the number of apoptotic cells because it possesses the ability to protect cells against glutamate, ischemia and staurosporine-induced cytotocity and apoptosis. METHODS: Huperzine A was administered intraperitoneally to male Wistar Albino rats (220-340 g of body weight) after moderate static clip compression (70 g for 60 s) of the spinal cord at T7 level. Neurological functions were assessed using the Basso-Beattle-Breshanan (BBB) motor rating scale until 3th and 7th days before perfusion, following which the spinal cord was harvested for histopathological examinations and apoptotic cell counts. RESULTS: Histopathological evaluations of the spinal cord of the control, trauma and huperzine A treated groups were evaluated. Control group showed normal neuronal and vascular structures of the spinal cord. However, in both trauma groups 3rd- and 7th-day perfusion showed extensive cavitation and hemorrhage, areas of necrosis and edema in gray matter, and degeneration in motor neurons along with patchy areas of necrotic and apoptotic cells. In the group treated with huperzine A, an increased number of normal cells was observed, along with a lower number of necrotic cells, with a significant reduction in the apoptotic cells (P<0.01). The administration of huperzine A improved post-trauma motor performance. Furthermore, BBB scores of all groups showed that there was an improvement of locomotor abilities in the treatment group as compared with the control. CONCLUSIONS: When compared with controls, huperzine A treatment demonstrates a significant reduction in the number of apoptotic cells. In addition, the group treated with huperzine A showed significant and appreciable neurological improvement in rats.