Coenzyme Q10 attenuates neurodegeneration in the cerebellum induced by chronic exposure to tramadol.

BACKGROUND: Chronic use of tramadol can cause neurotoxic effects and subsequently cause neurodegeneration in the cerebellum. The main damage mechanisms identified are oxidative stress and inflammation. Currently, we investigated the effects of coenzyme Q10 (CoQ10) in attenuates of neurodegeneration in the cerebellum induced by chronic exposure to tramadol. MATERIAL AND METHODS: Seventy-two male mature albino rats were allocated into four equal groups, including; non-treated group, CoQ10 group (which received CoQ10 at 200 mg/kg/day orally for three weeks), tramadol group (which received tramadol hydrochloride at 50 mg/kg/day orally for three weeks), and tramadol+CoQ10 group (which received tramadol and CoQ10 at the same doses as the previous groups). Tissue samples were obtained for stereological, immunohistochemical, biochemical, and molecular evaluations. Also, functional tests were performed to evaluate behavioral properties. RESULTS: We found a significant increase in stereological parameters, antioxidant factors (catalase, glutathione, and superoxide dismutase), and behavioral function scores in the tramadol+CoQ10 group compared to the tramadol group (p < 0.05). In addition, malondialdehyde levels, the density of apoptotic cells, as well as the expression of pro-inflammatory (tumor necrosis factor-alpha, interleukin 1 beta, and interleukin 6) and autophagy (lysosome-associated membrane protein 2, autophagy-related 5, beclin 1, and autophagy-related 12) genes were considerably reduced in the tramadol+CoQ10 group compared to the tramadol group (p < 0.05). CONCLUSION: We conclude that the administration of CoQ10 has neuroprotective effects in the cerebellum of rats that have chronic exposure to tramadol.

Quercetin in combination with hyperbaric oxygen therapy synergistically attenuates damage progression in traumatic spinal cord injury in a rat model.

BACKGROUND: Oxidative stress, inflammation and cell apoptosis are the most important destructive factors in the spread of damage following trauma to the spinal cord. Therefore, presently, we investigated the synergistic effects of quercetin along with hyperbaric oxygen therapy (HBOT) as strong antioxidant, anti-inflammatory and anti-apoptotic compounds in the recovery of traumatic spinal cord injury (TSCI) in a rat model. MATERIAL AND METHODS: Seventy-five male mature Sprague-Dawley rats allocated into 5 groups, including: Sham group (SG), TSCI group, Quercetin group (underwent TSCI and received quercetin), HBOT group (underwent TSCI and received HBOT), and Quercetin+ HBOT group (underwent TSCI and received quercetin plus HBOT). Finally, the spinal cord samples at the traumatic site were harvested and various characteristics were evaluated, including the total volumes of the spinal cord and its central cavity as well as the numerical density of neuron and glial cells by stereological method, oxidant (malondialdehyde; MDA) and antioxidant (glutathione; GSH, superoxide dismutase; SOD and catalase; CAT) factors by biochemical method, molecular levels of IL-10, TNF-α and IL-1ß by qRT-PCR method, and cell apoptosis by immunohistochemistry method against Caspase-3 antibody. Furthermore, Basso-Beattie-Bresnahan (BBB) and electromyography latency (EMG Latency) tests were performed to evaluate neurological functions. RESULTS: Findings demonstrated that the stereological characteristics, biochemical factors (except MDA), expression of IL-10 gene and behavioral functions were significantly better in Quercetin, HBOT and Quercetin+HBOT groups than TSCI group, and were greater in Quercetin+HBOT ones (P < 0.05). While MDA levels, expression of TNF-α and IL-1ß genes as well as the density of apoptotic cells significantly more decreased in Quercetin+HBOT group compared to other treated groups (P < 0.05). CONCLUSION: Overall, co-administration of quercetin with HBOT has synergistic neuroprotective effects in animals underwent TSCI.

Spontaneous intracerebral hemorrhage, initial computed tomography (CT) scan findings, clinical manifestations and possible risk factors.

Intracerebral hemorrhage is one of the types of stroke in patients with risk factors. In this study, we aimed to evaluate the initial computed tomography (CT) scan findings, clinical manifestations and possible risk factors of patients with intracerebral hemorrhage. This is a cross-sectional study that was performed in 2015-2022 on 900 patients with definite diagnosis of intracerebral hemorrhage. Data of patients were evaluated for patient's age, gender, clinical manifestations, primary radiologic signs in CT scan and possible risks factors for stroke. Lobar hemorrhage was the most common site of involvement (324 patients, 36%) followed by lenticular (putamen) (294 patients, 32.7%) and thalamus (135 patients, 15%). Among patients, 543 patients (60.3%) had hypertension, 81 patients (9%) had histories of anticoagulant. Hemorrhages in putamen were significantly more common in patients with hypertension (P<0.001) and lobar hemorrhages were significantly more common in patients with the use of anticoagulant drugs (P=0.033). The most common presentation of hemorrhagic stroke was decreased consciousness level (428 patients, 47.5%) followed by headache (343 patients, 38.1%), coma (81 patients, 9%) and seizure (48 patients, 5.4%). Evaluation of the relationships between patient's main symptoms and sites of involvement showed that patients with decreased consciousness as their most common symptom had more frequently diagnosed with lobar hemorrhage (54%) and putamen hemorrhage (30.4%) (P<0.001). Hypertension was the most common past medical history that was significantly related to hemorrhage in basal nuclei. Hemorrhages in putamen were common in hypertensive patients and lobar hemorrhages were common in patients with anticoagulant use.