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Showing 6 results for Caspase

Leila Khalaj, Habibollah Peirovi, Fariba Khaodagholi, Azadeh Abdi, Leila Dargahi, Fatemeh Mohagheghi, Abolhassan Ahmadiani,
Volume 14, Issue 1 (3-2010)

Introduction: Postoperative neurological deficit is the most devastating complication after thoracoabdominal aortic aneurysm repair. Despite demonstrated neuroprotective effects of estradiol, its protective efficacy against spinal cord ischemia-reperfusion and underlying mechanisms are not yet elucidated. Methods: Two groups, each of 10 New Zealand white male rabbits, were studied. Control group received sesame oil (vehicle) while the treatment group received 17-β-Estradiol Cypionate (1 mg/kg) dissolved in sesame oil, 30 minutes before abdominal aortic clamping for 18 minutes. A group of sham operated animals was also included, which consisted of 5 rabbits subjected to operative dissections without aortic occlusion. After 48 h reperfusion we investigated the efficacy of estradiol in attenuating the spinal cord ischemia-induced pathology through neurological, histopathological, and western blot assessments. Results: The results showed that administration of estradiol 30 minutes before induction of spinal cord ischemia in rabbits improved functional outcome and prevented the worsening pattern of neurological function over 48 hours. Near to normal histopathological outcome of lumbar part of spinal cords in these animals confirmed neuroprotective effects of estradiol. Estradiol also reduced spinal cord Heat shock protein 70 and cleaved caspase-3 in this ischemic context. Conclusion: Estradiol can be considered as a potential candidate to protect against spinal cord ischemiareperfusion- induced paraplegia resulting from thoracoabdominal aortic aneurysm repairs.
Azadeh Abdi, Fatemeh Mohagheghi, Homayoon Sadraei, Leila Dargahi, Leila Khalaj, Abolhassan Ahmadiani,
Volume 14, Issue 3 (10-2010)

Introduction: Evidence suggests that neuronal apoptosis in neurodegenerative diseases is correlated with inflammatory reactions. The beneficial or detrimental role of apoptosis in neuroinflammation is unclear. Elucidating this question may be helpful in management of neurodegenerative diseases. Since TNF-α is able to induce apoptosis as well as increased viability of the cells by activation of caspases or NF-kB, respectively, the question is what will happen if the balance between the two pathways is disturbed by inhibition of apoptosis. Methods: In this study, we used β–amyloid peptide (soluble Aβ monomer) injection into the Wistar male rat prefrontal cortex for induction of neuroinflammation in the hippocampus. Levels of TNF-α and caspase-3 were determined via western blot analysis. Using chronic intracerebroventricular administration of caspase inhibitors, z-VAD –fmk and z-DEVD-fmk, we inhibited apoptosis. Exploring consequences of apoptosis inhibition, activity of NF-kB was evaluated via western blotting. Results: After β–amyloid peptide injection we observed an increase in TNF-α and caspase3 as an inflammatory cytokine and apoptotic marker, respectively (P<0.001 and P<0.0001, respectively). As a consequences of apoptosis inhibition, nuclear NF-κB was decreased and cytosolic NF-κB was increased and these changes were significant compared to Aβ-injected group (P<0.001 and P<0.05, respectively). Conclusion: Caspase inhibition as an initiator of apoptosis, probably by attenuation of NF-kB activity, protect cells from abnormal survival and proliferation.
Mohammad Husein Abnosi, Malek Soleimani Mehranjani, Sayed Mohammad Ali Shariatzadeh, Majid Mahdiyeh Najafabadi, Laila Dehdehi,
Volume 15, Issue 3 (10-2011)

Introduction: In this study, the effect of para-nonylphenol as an environmental pollutant on viability, morphology and proliferation of bone marrow mesenchymal stem cells was investigated. Methods: Bone marrow mesenchymal stem cells of rat were treated with the 0.5, 1, 2.5, 3.5 and 5 μM of paranonylphenol for a period of 21 days, then the viability of the cells were estimated using trypan blue and MTT methods. After choosing the effective dose, the integration of the DNA was investigated using comet assay and agarose gel electrophoresis. Mechanisms of cell death were also investigated by TUNEL assay and presence of caspase activity. Results: The results showed that para-nonylphenol caused significant dose dependent reduction of viability and proliferation of the cells. Comet assay, agarose gel electrophoresis and TUNEL test showed that the DNA of the cells were damaged and broken after treatment with 0.5 and 2.5 μM of para-nonylphenol. In addition, activated caspase-3 was observed in the cytoplasm of treated cells. Conclusion: This study showed that a very low concentration of para-nonylphenol has drastic effects on bone marrow mesenchymal stem cells. This chemical is used in formulation of cosmetics and detergents and therfore may have detrimental effects on the viability and proliferation of stem cells.
Najmeh Katebi, Yasaman Razavi, Shabnam Zeighamy Alamdary, Shiva Irani , Fariba Khodagholi, Abbas Haghparast,
Volume 17, Issue 1 (3-2013)

Introduction: Nucleus accumbens (NAc) plays a critical role in neuronal reward circuits that are responsible for motivated and goal-directed behaviors. Some data suggest that morphine induces apoptosis in neurons, while other evidences show that morphine could have beneficial effects against neuronal cell death. This study was designed to evaluate the effect of morphine on apoptosis in the NAc in rat brain by assessing the changes in apoptotic factors. Methods: To investigate the effects of 3 different doses (0.5, 5 and 10 mg/kg) of morphine on induction of apoptotic factors in the NAc after its sub-chronic consumption, conditioned place preference paradigm was used in three groups of rats compared with the control group that received saline, and then the changes in apoptotic factors caspase-3, PARP and Bax/Bcl-2 ratio were assessed by western blot technique. Results: Our results showed that apoptotic factors increase in all three groups treated with morphine. In the nucleus accumbens, morphine induced significant increase (p<0.01) in caspase-3, PARP and Bax/Bcl-2 ratio, in the lowest dose (0.5 mg/kg) compared with the control group that received saline instead of morphine. Conclusion: Increase in apoptotic factors by low dose morphine in the nucleus accumbens of morphine-treated rats shows that morphine can affect the molecular mechanisms which interfere with apoptosis through one kind of its receptors with high affinity. However, with increase in dose of morphine, it seems that other kinds of opioid receptors have been involved which exert some neuroprotective effects of morphine against apoptosis.
Hassan Niknejad, Mahsa Khayat-Khoei, Ghasem Yazdanpanah, Habibollah Peirovi,
Volume 17, Issue 2 (7-2013)

Introduction: Amniotic membrane, the innermost layer of extra-embryonic tissue, contains mesenchymal and epithelial stem cells. The amniotic mesenchymal cells have the capability of inhibition of growth of cancer cells. In this research, the effects of amniotic epithelial cells on the viability of cancer cells and the role of apoptosis in this procedure were evaluated. Methods: Amniotic membrane derived epithelial cells were cultured for 24 hours and their supernatant was added to the culture of cancer cells (HeLa and MDA-MB-231) in volumes of 200, 400, 600 and 800 μl. Viability of cancer cell lines were measured by MTT assay after 24 hours. Also, the expression of caspase 3 and 8 (pro apoptotic proteins) was evaluated with immunocytochemistry. Analysis of data was performed using one-way analysis and post-Tukey test in ANOVA. Results: Viability of cancer cells were significantly decreased after culture with condition medium of amniotic epithelial cells in comparison to the control group. This decrease was dose-dependent and more significant at higher doses (600 and 800 μl). The expression of caspase-3 and caspase-8 was dose-dependently increased in cancer cells. Conclusion: The promising results of this study showed that amniotic epithelial cells have the capability to be investigated as a proper candidate for cancer therapy.
Ghorbangol Ashabi, Leila Khalaj,
Volume 19, Issue 4 (12-2015)

Introduction: Neurodegenerative diseases are progressive disorders that could impair neuronal functions and structures. Oxidative stress and mitochondrial dysfunction are involved in the etiology of neurodegenerative diseases such as Alzheimer’s disease, Parkinson’s disease and etc. Gemfibrozil is used as a therapeutic drug for hyperlipidemia. It has been shown that gemfibrozil is neuroprotective via modulation of mitochondrial biogenesis pathway under oxidative stress condition and in a sex-dependent manner. Materials and Methods: In this study, neuronal-like PC12 cells with were pretreated with different concentrations of gemfibrozil and H2O2, concomitantly. Results: In gemfibrozil pretreated groups, reduced level of caspase-3 and raised mitochondrial transcription factor A (TFAM) levels were detected. In contrast, adding fulvestrant, an Estradiol receptor antagonist, prevents the impact of gemfibrozil on oxidative stress condition, reducing its efficacy to protect the neurons against stress. Conclusion: Our results indicated the involvement of estradiol receptors in gemfibrozil neuroprotective mechanism, in diminishing oxidative stress-induced damage via reducing caspase-3 and inducing the level of TFAM that plays a crucial role in the mitochondrial biogenesis.

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