جستجوی مقالات مرتبط با کلیدواژه "بیماری پارکینسون" در نشریات گروه "زیست شناسی"

Parkinson's disease is associated with motor and cognitive disorders, so we investigated the administration of Eclipta prostrata hydroalcoholic extract on learning, memory, motor activity and oxidative stress in Parkinson's model.

50 adult Wistar rats were divided into five groups: control group, parkinsonian group and three groups treated with eucalyptus perstrata extract in three different concentrations of 50, 100 and 200 mg/kg. Induction of Parkinson's model was done by injecting 6-hydroxydopamine (6-OHDA). One day after the last gavage, motor tests were done. The shuttle box test was used to evaluate learning and avoidance memory. Oxidative stress was evaluated by malondialdehyde, glutathione peroxidase and thiol content.

7 days after the lesion in the MFB, after the administration of apomorphine, the rats turned 360 degrees in the right direction at a rate of more than 10 revolutions per minute. In the movement tests of the parkinsonian group, maintaining balance in rotarod (p<0.001), catalepsy (p<0.001), muscle stiffness (p<0.001), stride length (p<0.001) and avoidance memory (p<0.001) showed a significant difference to the control group. Also, Eclipta prostrata extract significantly improved all kinds of movement disorders caused by Parkinson's disease, and in doses of 50, 100, and 200, it improved memory in Parkinsonian rats (p<0.001). Also, the extract significantly increased the amount of thiol (p<0.001). and glutathione peroxidase (p<0.001) and decreased MDA in hippocampus and striatum tissue (p<0.001).

In general, we showed that the hydroalcoholic extract of Eclipta prostrata administered in the animal model of Parkinson's has a favorable effect on memory, learning, motor activity and oxidative stress of the brain.

Oxidative stress and neuroinflammation play a role in Parkinson's disease. Antioxidants and anti-inflammatories such as polyphenol compounds and flavonoids inhibit neuronal death. The aim of the present study is the effect of xanthone and 6-hydroxyflavone in Parkinson's disease in laboratory mice. Animals are cannulated by stereotaxic surgery and unilateral injection of 6-hydroxy-dopamine is performed in the dense area of ​​the substantia nigra (SNc) of the brain. Xanthone and 6-hydroxyflavone were injected intraperitoneally. Three weeks after surgery, movement evaluations and pseudo-anxiety and pseudo-depression behaviors were performed. Counting of all the neurons in the dense area of ​​the substantia nigra was done. Injection of 6-hydroxydopamine increased the number of apomorphine rotations. Catalysis time increased. Neurons in the substantia nigra decreased. 6-Hydroxyflavone (50 and 100 mg/kg) and xanthone (100 and 200 mg/kg) reduced vertigo and catalepsy. In the elevated plus shape maze test, 6-hydroxyflavone in doses of 25 and 50 mg/kg and xanthone in doses of 50 and 100 mg/kg increased motor activity. In the forced swimming test, xanthone in doses of 50, 100 and 200 mg/kg reduced immobility in parkinsonian rats. The number of substantia nigra neurons increased with the treatment of 6-hydroxyflavone in doses of 50 and 100 mg/kg and 200 mg/kg xanthone. Xanthone and 6-hydroxyflavone improved movement disorder and catalepsy and increased the number of nerve cells in the substantia nigra. Xanthon was able to reduce depression. Probably, part of these central protective effects are mediated by the antioxidant and anti-inflammatory effects of xanthone and 6-hydroxyflavone, which prevent cell death by reducing free radicals and inflammatory cytokines, and as a result, they improve cognitive and movement disorders.

Considering the role of oxidants in the pathogenesis of this disease, in this study, the effect of pycnogenol as an antioxidant on the improvement of motor function and anxiety behavior in the experimental model of Parkinson’s disease were assessed. Forty male NMRI mice were randomly divided into five groups (n=8 in each group): The control (saline) unilaterally received 3 μl of normal saline solution containing 0.1% ascorbic acid, as a solvent of 6-hydroxy dopamine (6-OHDA), into the left strianum. The treatment group received 6-OHDA toxin containing 1% ascorbic acid at a rate of 3 µg/µl in the left striatum and then received the distilled water, as pycnogenol solvent, via gavage for 7 days (the lesion group). The pycnogenol-treated groups received pycnogenol at doses of 10, 20, and 30 mg/kg via gavage for 7 days. The animals were stereotaxically operated to inject 6-OHDA toxin into the left striatum. Seven days after induction of Parkinson’s model, apomorphine was intraperitoneally used at dose of 0.5 mg/kg and the number of rotation of the animals was measured to confirm the damage to neurons in the striatum. Besides, the catalepsy or muscle stiffness by the bar test and the anxiety behavior by the plus maze test (EPM) were measured. The total number of rotations in apomorphine test showed a significant decrease in the groups receiving pycnogenol. Moreover, administration of pycnogenol significantly reduced catalepsy in pycnogenol-treated groups. The result of the anxiety behavior test demonstrated that the percentage of open arm time (OAT) and the number of open and close arm entries, as an indicator of the animal’s locomotor activity, significantly increased in the pycnogenol-treated groups. Pycnogenol with its antioxidant effect ameliorates movement deficit and reduces anxiety behavior in animal model of Parkinson’s disease..

In this study, the alteration of the Leucine-rich repeat kinase 2 (LRRK2) gene, as the most important gene involved in Parkinson's disease, was investigated using CRISPR-Cas editing technology.

Cloning the guide molecules of interest was performed using of gRNA CRISPR cloning kit (Catalog No. C8324K, Zaver Zist Azema). Two sets of forward and reversed gRNA oligonucleotides for exon 41 of the LRRK2 gene were designed using the CHOPCHOP CRISPR guide gRNA designing web software. Double-stranded DNA molecules were made according to standard instructions in the laboratory. 20 base-pair DNA segments were used to generate RNA-Cas-9 enzyme complex and then ligated into the Px459 CRISPR eukaryotic expression vector using Fermentas DNA ligase enzyme. Recombinant plasmids were transformed into E. coli DH5a host competent cells using of heat shock method.

findings by multiple PCR experiments and also DNA sequencing blast analysis showed successful cloning the segments of interest into CRISPR plasmids. Clear PCR bands were in agreement with expected values and DNA sequencing results showed 100% similarity. 

According to the results, development of CRISPR vector system may be used as a wide and powerful tool for editing and alteration of many encountered genes in different diseases such as Parkinson's disease.

Catalepsy or muscle rigidity is a neurological disease characterized by muscle stiffness or rigidity of muscles, organs decreased sensitivity to pain and stability regardless of external stimuli-known and one of the main symptoms of Parkinson's disease is considered. Due to the increasing levels of acetylcholine in the brain, treatment is focused on the use of muscarinic receptor antagonists. Despite relieve the symptoms, there are severe side effects. In this study, the effect of cinnamon extract on catalepsy in mice model of Parkinson's disease was conducted. Overall, 70 male mice (30 ± 2 g) were randomly divided into seven groups: control group, rotenone solvent, rotenone group and 4 groups of rotenone, subsequent doses 100, 200, 400 and 600 mg/kg cinnamon extract. To create models of Parkinson's disease, rotenone (2 mg/kg/ 48 h) was administered for 19 d and creating models of Parkinson's disease was evaluated. After verification of the model, different doses of cinnamon for 20 d (every 48 h) were injected intraperitoneally (IP). The effects of cinnamon extract on catalepsy was compared with other groups and the results were analyzed by ANOVA and Tukey test.  PP<0. 05). Cinnamon could reduce catalepsy in mice models of Parkinson's disease, probably due to antioxidant compounds and flavonoids and the impact of these compounds on the nervous system.