17 beta-estradiol oxidative stress attenuation and autophagy-induced dopaminergic neuroprotection

Objective: Degeneration of dopaminergic neurons in the substantia nigra of the brain stem is the main pathological aspect of Parkinson's disease [PD]. 17 beta-estradiol [E2] has neuroprotective effects on substantia nigra, however, the underlined mechanism is not well-known. In this study, we evaluated the neuroprotective effects of E2 in the ovariectomized 6-hydroxydopamine- [6-OHDA] rat model of PD

Materials and Methods: In this experimental study, all animals were ovariectomized to avoid any further bias in E2 levels and then these ovariectomized rats were randomly assigned into three experimental groups [10 rats in each group]: ovariectomized control group [OCG], ovariectomized degeneration group receiving 25 µg of 6-OHDA into the left corpus striatum [ODG], and ovariectomized E2 pretreatment group pretreated with 0.1 mgkg-1of 17 beta-estradiol for three days prior to the destruction of corpus striatum with 6-OHDA [OE2PTG]. The apomorphine behavioral test and Nissl staining were performed in all experimental groups. The expressions of Sequestosome-1 [P62], Unc- 51 like autophagy activating kinase [Ulk1], and microtubule-associated proteins 1A/1B light chain 3B [Lc3] genes were evaluated using reverse transcription- polymerase chain reaction [RT-PCR]

Results: E2 administration reduced the damages to the dopaminergic neurons of the substantia nigra. The motor behavior, the number of rotations, and histological tests in the treatment group showed the cell survival improvement in comparison with the control groups indicating that E2 can inhibit the neurodegeneration. P62 and Lc3 were expressed in all experimental groups while Ulk1 was not expressed in ODG group. Moreover, Ulk1 was expressed after the treatment with E2 in OE2PTG group

Conclusion: E2 prevents neurodegeneration in dopaminergic neurons of the midbrain by over-expression of Ulk1 gene and augmenting the induction of autophagy

Low level of autophagy-related gene 10 [ATG10] expression in the 6-hydroxydopamine rat model of Parkinson's disease

Background: Autophagy is a mechanism disassembling the damaged organelles from the cell. This study attempted to examine the expression of several autophagy-related genes in Parkinson's disease [PD] rat model

Methods: The male Wistar rats were divided into three groups as control, sham, and lesion. In the latter group, the PD rat model was induced by the injection of 6-hydroxydopamine in the striatum. The behavioral test was conducted one [baseline] and four weeks after the surgery through apomorphine hydrochloride. Then the RT-PCR technique was employed to evaluate the expressions of p62/SQSTM, autophagy-related genes [ATG]5, ATG12, ATG16L1, ATG10, as well as GAPDH and LC3

Results: By injecting apomorphine, the striatal lesion group showed a significant contralateral rotation at fourth week as compared to the baseline. The examination of p62, ATG5, ATG12, ATG16L1, and LC3 expressions using RT-PCR revealed that p62, ATG5, ATG12, LC3, and ATG16L1 were expressed in the substantia nigra of PD rat model, while ATG10 was not expressed

Conclusion: ATG10 expression is necessary for the initiation of autophagy. Thus, these results show that autophagy deregulation occurs in the initiation stages of the process in the rat model of PD

Decrease in cavity size and oligodendrocyte cell death using Neurosphere-Derived oligodendrocyte-like cells in spinal cord contusion model

Background: Oligodendrocyte cell death is among the important features of spinal cord injury, which appears within 15 min and occurs intensely for 4 h after injury, in the rat spinal contusion model. Accordingly, the number of oligodendrocytes progressively reduced within 24 h after injury. Administration of oligodendrocyte-like cells [OLCs] into the lesion area is one of the approaches to counterbalance this condition

Methods: Bone marrow stromal cells were transdifferentiated into neurospheres and then into neural stem cells and later were differentiated into OLCs using triiodothyronine and transplanted into the spinal cord contusion rats. The postinjury functional recovery was explored and compared with the control group using Basso-Beattie-Bresnahan and narrow beam behavioral tests. At the end of 12th week, spinal cord segments T12-L1 were histomorphologically studied by immunohistochemistry

Results: Motor improvement was more obvious during 2nd to 4th weeks and got less prominent during 4th to 12th weeks. Histomorphometric findings indicated that cavity formation decreased in epicenter of transplantation area in experimental groups in comparison with the control groups

Conclusion: The findings obtained in the present study showed that OLC therapy is a potential approach in the treatment of spinal cord traumatic injuries

Stem cell transplantation and functional recovery after spinal cord injury: a systematic review and meta-analysis / 대한해부학회지

Spinal cord injury is a significant cause of motor dysfunctions. There is no definite cure for it, and most of the therapeutic modalities are only symptomatic treatment. In this systematic review and meta-analysis, the effectiveness of stem cell therapy in the treatment of the spinal cord injuries in animal models was studied and evaluated. A systematic search through medical databases by using appropriate keywords was conducted. The relevant reports were reviewed in order to find out cases in which inclusion and exclusion criteria had been fulfilled. Finally, 89 articles have been considered, from which 28 had sufficient data for performing statistical analyses. The findings showed a significant improvement in motor functions after cell therapy. The outcome was strongly related to the number of transplanted cells, site of injury, chronicity of the injury, type of the damage, and the induction of immune-suppression. According to our data, improvements in functional recovery after stem cell therapy in the treatment of spinal cord injury in animal models was noticeable, but its outcome is strongly related to the site of injury, number of transplanted cells, and type of transplanted cells.

Di-[2-ethylhexyl] phthalate-induced hippocampus-derived neural stem cells proliferation

The brain and spinal cord have a limited capacity for self-repair under damaged conditions. One of the best options to overcome these limitations involves the use of phytochemicals as potential therapeutic agents. In this study, we have aimed to investigate the effects of di-[2-ethylhexyl] phthalate [DEHP] on hippocampus-derived neural stem cells [NSCs] proliferation to search phytochemical candidates for possible treatment of neurological diseases using endogenous capacity. In this experimental study, neonatal rat hippocampus-derived NSCs were cultured and treated with various concentrations of DEHP [0, 100, 200, 400 and 600 micro M] and Cirsium vulgare [C. vulgare] hydroethanolic extract [0, 200, 400, 600, 800 and 1000 micro g/ml] for 48 hours under in vitro conditions. Cell proliferation rates and quantitative Sox2 gene expression were evaluated using MTT assay and real-time reverse transcription polymerase chain reaction [RT-PCR]. We observed the highest average growth rate in the 400 micro M DEHP and 800 micro g/ml C. vulgare extract treated groups. Sox2 expression in the DEHP-treated NSCs significantly increased compared to the control group. Gas chromatography/mass spectrometry [GC/ MS] results demonstrated that the active ingredients that naturally occurred in the C. vulgare hydroethanolic extract were 2-ethyl-1-hexanamine, n-heptacosane, 1-cyclopentanecarboxylic acid, 1-heptadecanamine, 2,6-octadien-1-ol,2,6,10,14,18,22-tetracosahexaene, and DEHP. DEHP profoundly stimulated NSCs proliferation through Sox2 gene overexpression. These results provide and opportunity for further use of the C. vulgure phytochemicals for prevention and/or treatment of neurological diseases via phytochemical mediated-proliferation of endogenous adult NSCs

Case report: a case report on variation in bifurcation of brachial artery

Variations in arterial anatomy are less frequent, contrary to the venous system, and most of these variations affect visceral arteries. Variations in the brachial artery are the most frequently reported and so far a minimum of six different patterns have been described. The most common of these patterns is the superficial brachial artery, which lies superficially to the median nerve. Much less prevalent is the high origin of the radial artery [brachioradial artery] or the existence of a doubled brachial artery [accessory brachial artery]. The current study presents a pattern of brachial artery variation which was previously undescribed. During dissection of the right upper limb of a 50 year-old male embalmed cadaver, the bifurcation of the brachial artery in the proximal portion of the middle third of the arm was observed. In this case, the medial branch reaches the medial aspect of the arm, posterior to the median nerve. Afterwards, this medial branch redirects laterally and crosses the median nerve again, this time lying anterior to the nerve till it reaches the lateral aspect of the arm. At the elbow level, the medial branch originates from the radial artery. The lateral branch of the brachial artery remains lateral to the median nerve and continues as ulnar artery and originates from the interosseous artery. It was also observed that the left brachial artery was smaller in size, and bifurcated high in the arm into the superficial radial and ulnar arteries. It was also interesting to note that the common interosseous artery was originated from the left radial artery in the cubital fossa, which descended deep to pronator teres where it was divided into the anterior and posterior interosseous arteries. These variations are discussed comprehensively and compared with the previous reports. Also, it is asserted how clinically the findings are significant

case report: rare communication of Ansa Cervicalis

During the past few years, researchers and practitioners have developed novel techniques, using ansa cervicalis to innervate muscles of the larynx paralyzed due to surgical procedures carried out in the chest and neck areas. During routine dissection of a middle-age male cadaver, an unusual course of the superior root of the ansa cervicalis was observed. In this case, the superior root of the ansa cervicalis fused with the vagus and ran within the carotid sheath, and then joined the inferior root forming the ansa cervicalis in the anterior wall of the carotid sheath. The study of this case will add to our current knowledge of ansa cervicalis and thus aid prevention of injury to the nerve during various surgical procedures