Showing 4 results for Sepehri
Gholamreza Sepehri, Mohammad Naser Shafeiee,
Volume 10, Issue 1 (1-2006)
Abstract
The present study was performed to evaluate the analgesic effect of morphine microinjection into the cuneiformis nucleus (CnF) and the effect of inactivation of this area by lidocaine on pain modulation. Rats were anaesthetized by thiopental (45-60 mg/kg/i.p.) and placed in a stereotaxic instrument, and then a guide cannula was implanted just one mm above the CnF. Following surgery and recovery period, various doses of morphine (10, 20 and 40 µg/0.5 µl saline) and lidocaine 5% (0.5 µl) were microinjected into the CnF. Antinociceptive response was measured by tail flick latency (TFL) and maximal possible effect (% MPE) for 25 min at 5-min intervals, before and after any injection in control and experimental groups. The results of this study showed that morphine microinjection into the CnF increased TFL in a dose-dependent manner. TFL was also increased significantly after lidocaine microinjection. However, co-microinjection of morphine and lidocaine increased TFL which was less than morphine microinjection alone. The intravenous morphine injection with lidocaine microinjection increased TFL significantly, as compared to morphine microinjection. These effects were reversed by naloxone administration. In summary, the results of this study showed that morphine microinjection into the CnF caused a significant analgesic response which indicates that CnF may be involved in pain modulation.
Delaram Eslimi, Houri Sepehri, Yasaman Rassouli, Samideh Khoei, Bahram Goliaei,
Volume 12, Issue 3 (7-2008)
Abstract
Background: Pectic acid extracted from plants increases the secretion of prolactin (PRL) when injected intravenously into ewes or fed to rats. Fragments of ewe hypophysis and lactating rabbit mammary gland incubated in vitro in the presence of pectic acid secreted more PRL and caseins compared to the controls. However, it is not known whether pectic acid directly stimulates PRL secretion in pituitary or interference of factors from hypophysis is required for this process. Methods: GH3/B6 cells, a clonal strain of rat pituitary, were cultured and incubated with pectic acid (2.5-100 mg/mL). The integrity of cells was examined under pectic acid treatment microscopically. Controls or pectic acid treated cells were assayed for their ability to produce PRL. The PRL was assayed by Western-blotting and Radioimmunoassay. Results: pectic acid did not have any significant effect on the viability of cells. After being incubated with pectic acid, the cells started to become circular and protuberant shape. The maximum stimulation and PRL secretion occurred at 100 mg/mL concentration within 30 min of incubation with pectic acid. Conclusion: pectic acid could stimulate the release of PRL in GH3/B6 cells in the short-term incubation. This result suggested that pectic acid is a non-toxic agent that could directly stimulate PRL secretion in pituitary cells without any interference of hypophysis.
Farnoosh Attari, Houri Sepehri, Ladan Delphi, Bahram Goliaei,
Volume 13, Issue 4 (10-2009)
Abstract
Background: Pectin is composed of complex polysaccharides that can inhibit cancer metastasis and proliferation with no evidence of toxicity. In the present study, the apoptotic and necrotic effects of pectic acid (PA) on the rat pituitary GH3/B6 tumor cells has been investigated. Methods: GH3/B6 cells were cultured in the Ham’s F12 medium enriched with 15% horse serum and 2.5% fetal bovine serum for 3 days. Then, they were treated by various amounts of PA in different periods (6, 24 and 48 hours). Bromocriptine was used as positive control and the cell viability was detected by MTT test. The nuclear morphology of cells was explored by florescent stains including acridine orange (AO)/ethidium bromide (EB). In addition, percentages of apoptotic and necrotic cells were studied with triphosphate nick-end labeling (TUNEL) assay, cell cycle analysis and propidium iodide (PI) staining. Results: Long-term incubation with PA results in increased cell death and DNA damage as detected by MTT assay and AO/EB staining. TUNEL assay showed that PA (100 µg/ml to 1 mg/ml) could induce apoptosis in a dose-dependent manner, while higher concentrations of PA (2.5 and 5 mg/ml) induced necrosis which was confirmed by PI staining. Furthermore, cell cycle analysis indicated that PA induced sub G1 events, and DNA fragmentation was also correlated with the number of the apoptotic cells. Conclusion: It can be concluded that PA is responsible for apoptosis in the rat pituitary tumor cells. Therefore, one may suggest that this group of polysaccharides can be used in treatment of pituitary tumors.
Ali Sepehrinezhad, Sajad Sahab Negah, Navid Pousti, Sajjad Mollaei,
Volume 28, Issue 0 (Supplementary 2024)
Abstract
Introduction: Coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is characterized by respiratory failure, pneumonia, coagulation, and multiorgan failure due to deregulation of cytokine release. Inflammasome activation has been reported with tissue injury and increased disease severity. Here, we conducted a bioinformatic analysis to predict possible cellular and molecular mechanisms of inflammasome activation-induced cell injury/death in COVID-19.
Methods and Materials: All genes- associated with SARS-CoV-2 and inflammasome were extracted from GeneWeaver. Afterward, common genes were selected for further enrichment analysis. Common genes were uploaded into the ToppGene database to predict significant molecular functions, biological processes, Cellular components, signaling pathways, and microRNAs for both SARS-CoV2 and inflammasome. Cytoscape was also used to reconstruct the drug-genetic network for shared genes.
Results: Our results demonstrated that 62 genes were related to inflammasome, and 2379 genes were associated with SARS-CoV-2. Among these gene sets, nine genes such as tumor necrosis factor, cathepsin B, baculoviral IAP repeat containing 3, interleukin 6, absent in melanoma 2, leptin receptor, NLR family pyrin domain containing 1, nucleotide-binding oligomerization domain containing 1, and signal transducer and activator of transcription one were shared between inflammasome and COVID-19. NOD-like receptor signaling, nucleotide-binding domain leucine-rich repeat-containing receptor NLR signaling, TNF-related weak inducer of apoptosis TWEAK signaling, SARS-CoV2 innate immunity evasion and cell-specific immune, and toll-like receptor signaling were the most significant involved pathways in pyroptosis following COVID-19. The external side of the plasma membrane, membrane raft, ISGF3 complex, AIM2 inflammasome complex, and endolysosome lumen were the main cellular components that may disrupt following inflammasome activation in COVID-19.
Conclusion and Discussion: Notably, our findings predicted some microRNAs and revealed central signaling cascades following inflammasome activity, which may benefit future therapeutic targets in COVID-19.
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