Investigation of miR-26b and miR-27b expressions and the effect of quercetin on fibrosis in experimental pulmonary fibrosis.

In this study, investigation of the effects of Quercetin on Bleomycin-induced pulmonary fibrosis and fibrosis-associated molecules miR-26b and miR-27b was aimed. Control group was given 10% saline on the 0th day, and saline was administered for 21 days starting from the 8th day. Group 2 was given 50 mg/kg Quercetin for 21 days starting from the 8th day. Group 3 was given 10 mg/kg Bleomycin Sulfate on day 0, and sacrificed on the 22nd and 29th day. Group 4 was given 10 mg/kg Bleomycin Sulfate on the 0th day, and was given 50 mg/kg Quercetin for 14 days, and 21 days starting from day 8. Lung tissues were examined using light and electron microscopic, immunohistochemical and molecular biological methods. Injury groups revealed impaired alveolar structure, collagen accumulation and increased inflammatory cells in interalveolar septum. Fibrotic response was decreased and the alveolar structure was improved with Quercetin treatment. α-SMA expressions were higher in the injury groups, but lower in the treatment groups compared to the injury groups. E-cadherin expressions were decreased in the injury groups and showed stronger immunoreactivity in the treatment groups compared to the injury groups. miR-26b and miR-27b expressions were lower in the injury groups than the control groups, and higher in the treatment groups than the injury groups. Quercetin can be considered as a new treatment agent in the idiopathic pulmonary fibrosis, since it increases the expression levels of miR-26b and miR-27b which decrease in fibrosis, and has therapeutic effects on the histopathological changes.

Investigation of the protective effect of long-term exercise on molecular pathways and behaviours in scopolamine induced alzheimer's disease-like condition.

Despite research, the role of exercise in treatment and prevention of neurodegenerative diseases remains unclear. Our study, investigated that protective effect of treadmill exercise on molecular pathways and cognitive behaviours in a scopolamine-induced model of Alzheimer's disease. For that purpose, male Balb/c mice subjected to exercise for 12 weeks. During the last 4 weeks of exercise, mice were given an injection of scopolamine (2 mg/kg). Following injection, open field test and Morris water maze test were used to assess emotional-cognitive behaviour. Hippocampus and prefrontal cortex of mice were isolated, and levels of BDNF, TrkB, and p-GSK3ßSer389 were assessed by western blotting, and levels of APP and Aß-40 were analysed by immunohistochemistry. In our study, scopolamine administration increased anxiety-like behaviour in open field test, while negatively affecting spatial learning and memory in Morris water maze test. We found that exercise had a protective effect against cognitive and emotional decline. Scopolamine decreased levels of p-GSK3ßSer389, BDNF in hippocampus and prefrontal cortex.Whereas TrkB decreased in hippocampus and increased in prefrontal cortex. There was an increase in p-GSK3ßSer389, BDNF, TrkB in the hippocampus, and p-GSK3ßSer389, BDNF in the prefrontal cortex in the exercise + scopolamine group. Immunohistochemical analysis showed that scopolamine administration increased APP and Aß-40 in hippocampus and prefrontal cortex in neuronal and perineuronal areas whereas Aß-40 and APP were reduced in exercise + scopolamine groups. In conclusion, long-term exercise may have a protective effect against scopolamine-induced impairments in cognitive-emotional behaviour. It can be suggested that this protective effect is mediated by increased BDNF levels and GSK3ßSer389 phosphorylation.

Distribution of Aquaporin-4 channels in hippocampus and prefrontal cortex in mk-801-treated balb/c mice.

Functional disorders of the glymphatic system and Aquaporin-4 (AQP-4) channels take part in the pathophysiology of neurodegenerative disease. The aim of this study was to describe the distribution of AQP-4 channels in the prefrontal cortex and hippocampus in a mouse model of NMDA receptor blocking agent-induced schizophrenia-like behavior model. NMDA receptor antagonist MK-801 was used to produce the experimental schizophrenia model. MK-801 injections were administered for eleven days to Balb/c mice intraperitoneally. Beginning from the sixth day of injection, the spatial learning and memory of the mice were tested by the Morris water maze (MWM) task. A group of mice was injected with MK-801 for ten days without the MWM task. Hippocampus and prefrontal specimens were collected from this group. Tissue samples were stained immunohistochemically and AQP-4 channels were examined by electron microscope. Time to find the platform was significantly longer at MK-801 injected group than the control group at the MWM task. Also, time spent at the target quadrant by the MK-801 group was shorter compared to the control group. AQP-4 expression increased significantly at MK-801 group glial cells, neuronal perikaryon, perineuronal and pericapillary spaces. In the MK-801 group, there was remarkable damage in neurons and glial cells. Increased AQP-4 channel expression and neurodegeneration at the MK-801 group induced with schizophrenia-like behavior model. MK-801 induced NMDA receptor blockade causes a decline in cognitive and memory functions. Increased AQP-4 expression at the prefrontal cortex and hippocampus to elicit and transport products of synaptic neurotransmitters and end metabolites is suggested.

Effects of Theranekron and alpha-lipoic acid combined treatment on GAP-43 and Krox-20 gene expressions and inflammation markers in peripheral nerve injury.

Peripheral nerve injury (PNI) is a major health problem that results in loss of motor and sensory functions. In treatment of PNI, various methods such as anastomosis, nerve grafts, nonneural tissue grafts, and nerve conduits are applied. In the present study, it was aimed to investigate the effects of Theranekron and Alpha-lipoic acid (ALA) combined treatment on nerve healing in experimental PNI by using histomorphometric, electron microscopic, immunohistochemical and molecular biological methods. Sixty-two Wistar rats were divided into six groups; the normal control group, sham operation group, experimental control group having a crush type injury with no treatment, Theranekron treatment group, ALA treatment group and Theranekron+ALA combined treatment group. Sciatic nerve tissue samples were obtained on days 1, 7 and 14 following injury in all groups. GAP-43 expression was upregulated in all PNI received groups compared to the control group. Krox-20 expression was downregulated in all groups that received PNI compared to the control group. While intensely positive TNF-α and IL-6 expressions were observed up to the 1st to the 14th day for the experimental control group, these expressions were seen as "weakly positive" in the treatment groups from the 1st day to the 14th day. The number of myelinated fibers was higher in the control and sham operation groups. Additionally, the number of myelinated nerve fibers increased in the combined treatment group. In conclusion, these findings suggest that combined therapy of Theranekron and ALA promotes structural recovery and it should be considered as an effective treatment protocol following PNI.