Tehran University Medical Journal

---

Background: Parkinson's disease (PD) is a degenerative neurodopaminergic disease in nigrostriatum pathway of animals and human, the resultant loss of nerve terminals accompanied by dopamine-glutamate and other related neurotransmitters-imbalances in this pathway are responsible for most of the movement abnormalities. Increasing evidence suggests that an inflammatory reaction accompanies the pathological processes caused by Cyclooxygenase-2 (COX-2) seen in many neurodegenerative disorders, including PD. These findings have not indicated any evidence based on the effect of selective and non selective COX-2 inhibitors on the rigidity of PD.
Methods: The rats left substantia nigra pars compacta (SNc) was destroyed using the electrical lesion thus PD model was created. Then oral aspirin and celecoxib (200, 400 mg/kg) were administrated to parkinsonian rats acutely and then the rigidity was evaluated using Murprogo's Method.
Results: Both compounds were able to decrease the rigidity of parkinsonian rats (p<0.05) respectively but selective cox-2 inhibitor (celecoxib) was found more effective and potent than that of non selective cox-2 inhibitor (aspirin). Conclusion: The findings suggest that COX-2 inhibition decreases the rigidity of PD in the animal model. Therefore, as results of the study COX-2 inhibition was shown good evidence based on the use of aspirin and celecoxib and PD affiliated rigidity improvement that this can be beneficial and interest for neuroscientists. These findings are additional pharmacological and medicinal information to further assess of non steroidal anti inflammatory drugs (NSAIDs) as alternative therapeutic agents for PD affiliated rigidity treatment. Further experiments seem to be necessary to complete this research such as investigation the effects of NSAIDs on the striatum neurotransmission pathway

---

Normal 0 false false false EN-US X-NONE AR-SA MicrosoftInternetExplorer4 Background: Cyclooxygenase 2 is a key enzyme which converts arachidonic acid into prostaglandins. Cyclooxygenase 2 is triggered by inflammatory stimuli, such as cytokines. Its expression increases in tumors and Alzheimer's disease and ovarian hyperstimulation syndrome. Polycystic ovarian syndrome is a heterogeneous disease characterized by pathological angiogenesis and chronic anovulation. In the present study, the probable role of cyclooxygenase 2 in Wistar rats with polycystic ovarian syndrome was investigated.
Methods:  Thirty female Wistar rats (170-200 gr) were equally divided into three groups: 2 mg estradiol valerate was intramuscularly administered to each rat in the experiment group or group 1 the rats in group 2 were regarded as the sham group and received sesame oil injections and group 3 or the control group received no injections. After 60 days of treatment, animals were anaesthetized with chloroform and killed by decapitation. Ovaries were collected for histological and immunohistochemical evaluations. All the experiments were repeated three times.
Results:  Morphologically, ovaries from the control group exhibited follicles in various stages of development and many fresh corpus luteum. In estradiol valerate group small follicles in early development were observed in addition to follicles showing evidence of atresia and many large cysts with thickened theca cell layer. Corpus luteum was rare or absent in group 2. The immunohistochemical analysis for cyclooxygenase 2 expression showed an increased expression of cyclooxygenase 2 enzyme in group 1.
Conclusion: The results suggested the involvement of cyclooxygenase 2 in the progression to polycystic ovarian syndrome in a rat model.

---

Background: Transitional Cell Carcinoma (TCC) is the most common type of urinary bladder cancer. Cyclooxygenase-2 (COX-2), a key enzyme in prostaglandins biosynthesis, has been introduced as a new candidate for targeted therapy in this cancer. In this study, we investigated the expression of COX-2 in urinary bladder TCCs and its relationship with clinicopathological parameters such as tumor grade and stage.

Methods: This cross-sectional study was performed in the Pathology department of Sina Hospital in Tehran, Iran during 2006-2011. Pathology reports of patients with definite diagnosis of urinary bladder TCCs who had undergone Transurethral Resection (TUR) were reviewed and 40 cases were selected. Subsequently, COX-2 expression was assessed immunohistochemically by the examination of paraffin embedded tissue blocks. Staining in more than 5% of tumor cells was considered as positive expression.

Results: COX-2 was expressed in 52.5% of the patients. High-grade tumors revealed a higher (87.5%) COX-2 expression versus other grades of the lesions and there was a statistically significant difference in COX-2 expression between them (P<0.001). Patients' age was also related to the expression of this marker (P=0.03). In contrast, this marker did not correlate with other characteristics including gender, lymphatic invasion or tumor stage. In addition, perineurial or vascular invasions were not detected in any of the patients.

Conclusion: COX-2 expression was seen in more than half of our patients and it had a marked relation to tumor differentiation. Accordingly, this molecule may be a useful tumor marker in the assessment of urinary bladder cancers.