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کاربرد نوع شرط:
- جایگاه : پژوهشی
- مجله: Iranian Journal of Basic Medical Sciences
- نوع مقاله: Journal Article
- کلمات کلیدی: Heart rate,Angiotensin II,Resistin,Arterial Pressure,Corticotrophin-releasing hormone,L-Glutamate,Paraventricular hypothalamic nucleus
- چکیده:
- چکیده انگلیسی: Objective(s): Resistin, as a 12.5 kDa cysteine-rich polypeptide, is expressed in hypothalamus and regulates sympathetic nerve activity. It is associated with obesity, metabolic syndrome and cardiovascular diseases. In this study, we investigated the neural pathway of cardiovascular responses induced by injection of resistin into paraventricular nucleus (PVN) with rostral ventrolateral medulla (RVLM).
Materials and Methods: Adult male rats were anesthetized with urethane (1.4 g/kg intraperitoneally). Resistin (3 µg/1 µl/rat) was first injected into PVN, and the glutamatergic, corticotrophin-releasing factor (CRF)-ergic and angiotensinogenic transmission was inhibited by injecting of their antagonist in RVLM. Arterial pressure (AP) and heart rate (HR) were monitored before and after the injection.
Results: The results showed that resistin injection into PVN significantly increased AP and HR compared to control group and prior to its injection (P<0.05). Injection of AP5 ((2R)-amino-5-phosphonovaleric acid; (2R)-amino-5-phosphonopentanoate) (50 nM/rat), losartan (10 nM/rat) and astressin (50 nM/rat) into RVLM reduced cardiovascular responses produced by injected resistin into PVN. Injection of AP5+losartan or astressin+losartan or astressin+AP5 into RVLM could significantly reduce cardiovascular responses produced by resistin compared to before injection (P<0.05). Furthermore, the depressor responses generated by AP5+losartan injected into RVLM were significantly stronger than the depressor responses generated by AP5+astressin and/or astressin+losartan injected into RVLM (P<0.05).
Conclusion: It can be concluded that glutamatergic and CRFergic transmissions have crucial contribution to cardiovascular responses produced by resistin. The results provided new and potentially important insight regarding neural transmission when the plasma level of resistin increases; this reveals the role of resistin in cardiovascular responses such as metabolic syndrome and hypertension.- انتشار مقاله: 22-02-1398
- نویسندگان: Abolfazl Akbari,Gholamali Jelodar
- مشاهده
- جایگاه : پژوهشی
- مجله: Iranian Journal of Basic Medical Sciences
- نوع مقاله: Journal Article
- کلمات کلیدی: Heart rate,Angiotensin II,Resistin,Arterial Pressure,Corticotrophin-releasing hormone,L-Glutamate,Paraventricular hypothalamic nucleus
- چکیده:
- چکیده انگلیسی: Objective(s): Resistin, as a 12.5 kDa cysteine-rich polypeptide, is expressed in hypothalamus and regulates sympathetic nerve activity. It is associated with obesity, metabolic syndrome and cardiovascular diseases. In this study, we investigated the neural pathway of cardiovascular responses induced by injection of resistin into paraventricular nucleus (PVN) with rostral ventrolateral medulla (RVLM).
Materials and Methods: Adult male rats were anesthetized with urethane (1.4 g/kg intraperitoneally). Resistin (3 µg/1 µl/rat) was first injected into PVN, and the glutamatergic, corticotrophin-releasing factor (CRF)-ergic and angiotensinogenic transmission was inhibited by injecting of their antagonist in RVLM. Arterial pressure (AP) and heart rate (HR) were monitored before and after the injection.
Results: The results showed that resistin injection into PVN significantly increased AP and HR compared to control group and prior to its injection (P<0.05). Injection of AP5 ((2R)-amino-5-phosphonovaleric acid; (2R)-amino-5-phosphonopentanoate) (50 nM/rat), losartan (10 nM/rat) and astressin (50 nM/rat) into RVLM reduced cardiovascular responses produced by injected resistin into PVN. Injection of AP5+losartan or astressin+losartan or astressin+AP5 into RVLM could significantly reduce cardiovascular responses produced by resistin compared to before injection (P<0.05). Furthermore, the depressor responses generated by AP5+losartan injected into RVLM were significantly stronger than the depressor responses generated by AP5+astressin and/or astressin+losartan injected into RVLM (P<0.05).
Conclusion: It can be concluded that glutamatergic and CRFergic transmissions have crucial contribution to cardiovascular responses produced by resistin. The results provided new and potentially important insight regarding neural transmission when the plasma level of resistin increases; this reveals the role of resistin in cardiovascular responses such as metabolic syndrome and hypertension.- انتشار مقاله: 22-02-1398
- نویسندگان: Abolfazl Akbari,Gholamali Jelodar
- مشاهده
- جایگاه : پژوهشی
- مجله: Iranian Journal of Basic Medical Sciences
- نوع مقاله: Journal Article
- کلمات کلیدی: Cataract,Mutation,Congenital,Connexine 50 gene,GJA8
- چکیده:
- چکیده انگلیسی: Objective(s): Childhood cataract is a genetically heterogeneous eye disorder that results in visual impairment. The aim of this study was to identify the genetic mutations of connexin 50 gene among Iranian families suffered from autosomal dominant congenital cataracts (ADCC).
Materials and Methods: Families, having at least two members with bilateral familial congenital cataract, were selected for the study. Probands were evaluated by detailed ophthalmologist’s examination, and the pedigree analysis was performed. PCR amplifications were performed corresponding to coding region and intron-exon boundaries of GJA8, a candidate gene responsible for ADCC. PCR products were subjected to bidirectional sequencing, and the co-segregation of identified mutations was examined and finally, the impact of identified mutations on biological functions of GJA8 was predicted by in silico examination.
Results: Three different genetic alterations, including c.130G>A (p.V44M), c.301G>T (p.R101L) and c.134G>T (p.W45L) in GJA8 gene were detected among three probands. Two identified mutations, W45L and V44M have been already reported, while the R101L is a novel mutation and its co-segregation was examined. This mutation was exclusively detected in the ADCC and could not be found among the healthy control group. The result of bioinformatic studies of R101L mutation predicted that this amino acid substitution within GJA8 could be a disease-afflicting mutation due to its potential effect on the protein structure and biological function.
Conclusion: Our results suggest that mutations of lens connexin genes such as GJA8 gene could be one of the major mechanisms of cataract development, at least in a significant proportion of Iranian patients with ADCC.- انتشار مقاله: 11-12-1395
- نویسندگان: Masoumeh Mohebi,Saeed Chenari,Abolfazl Akbari,Fariba Ghassemi,Mehran Zarei-Ghanavati,Ghasem Fakhraie,Nahid Babaie,Mansour Heidari
- مشاهده
- جایگاه : پژوهشی
- مجله: Iranian Journal of Basic Medical Sciences
- نوع مقاله: Journal Article
- کلمات کلیدی: Valproic acid,cervical cancer,HPV,E-cadherin
- چکیده:
- چکیده انگلیسی: Objective(s): Valproic acid (VPA) has proven to be as one of the most promising useful drug with anticancer properties.In this study, we investigate the VPA effects on E-cadherin expression in HeLa, TC1, MKN45, and HCT116 cell lines. This study assesses the effects of VPA on human papillomavirus E7 expression in HPV positive cell lines. Materials and Methods: Cell lines were treated by2 mmol/l VPA and expression of E-cadherin and E7 was analyzed by quantitative real-time PCR. Student’s t test and ANOVA were used to determine changes in expression levels. Results:The results revealed that mean of E-cadherin expression is increased by VPA 1.8 times in HCT116 and MKN45 cell lines, also the mean of E-cadherin mRNA levels is up-regulated 2.9 times in HeLa and TC1 cell lines. So, E-cadherin augmentation induced by VPA in HeLa and TC-1, HPV positive cell lines, is higher than HPV negative cell lines MKN45 and HCT116. The mean of HPV E7 expression is decreased by VPA, 4.6 times in in HeLa and TC-1 cell lines. Conclusion: This study demonstrates that re-expression of E-cadherin by VPA in HPV positive cell lines is more than HPV negative cell lines. Whereas, HPV E7 reduces the expression of E-cadherin, reduction of HPV E7 expression by VPA is related to more augmentation of E-cadherin in HPV positive cell lines. So, this study demonstrates that VPA has more anticancer properties in HPV positive cell lines, and could potentially be a promising candidate for cervical cancer treatment.
- انتشار مقاله: 12-04-1395
- نویسندگان: Ebrahim Faghihloo,Abolfazl Akbari,Fatemeh Adjaminezhad-Fard,Talat Mokhtari-Azad
- مشاهده
- جایگاه : پژوهشی
- مجله: Iranian Journal of Basic Medical Sciences
- نوع مقاله: Journal Article
- کلمات کلیدی: Colon cancer,Oncogenic and suppressor micro RNAs (miRNAs),SD-208,TGF-β receptor 1 (TGβRI) kinase inhibitor
- چکیده:
- چکیده انگلیسی:
Objective(s):Transforming growth factor-β(TGF-β) is involved in colorectal cancer (CRC). The SD-208 acts as an anti-cancer agent in different malignancies via TGF-β signaling. This work aims to show the effect of manipulation of TGF-β signaling on some miRNAs implicated in CRC.
Materials and Methods: We investigated the effects of SD-208 on SW-48, a colon adenocarcinoma cell line. The cell line was treated with 0.5, 1 and 2 μM concentrations of SD-208. Then, the xenograft model of colon cancer was established by subcutaneous inoculation of SW-48 cell line into the nude mice. The animals were treated with SD-208 for three weeks. A quantitative real-time PCR was carried out for expression level analysis of selected oncogenic (miR-21, 31, 20a and 135b) and suppressor-miRNAs (let7-g, miR-133b, 145 and 200c). Data were analyzed using the 2-∆∆CT method through student’s t-test via the GraphPad Prism software.
Results: Our results revealed that SD-208 could significantly down-regulate the expression of one key onco-miRNA, miR-135b, in either SW-48 colon cells (P=0.006) or tumors orthotopically implanted in nude mice (P=0.018). Our in silico study also predicted that SD-208 could modulate the expression of potential downstream tumor suppressor targets of the miR135b.
Conclusion: Our data provide novel evidence that anticancer effects of SD-208 (and likely other TGF-β inhibitors) may be owing to their ability to regulate miRNAs expression.- انتشار مقاله: 13-07-1394
- نویسندگان: Abolfazl Akbari,Mohammad Hossein Ghahremani,Gholam Reza Mobini,Mahdi Abastabar,Javad Akhtari,Manzar Bolhassani,Mansour Heidari
- مشاهده
- جایگاه : پژوهشی
- مجله: Current Medical Mycology
- نوع مقاله: Journal Article
- کلمات کلیدی: cancer,Mycotoxin,HeLa cells,Patulin
- چکیده:
- چکیده انگلیسی: Background and Purpose: Patulin is a mycotoxin produced by some molds,especially Aspergillus and Penicilium, and is responsible for mycotoxicosis in animals and humans.There is still not very detailed data about the anti-cancer potency of patulin, but some reports demonstrated that it induces cellular apoptosis and toxicity.
Materials and Methods: To determine the efficacy of patulin as a therapeutic strategy for cervical and colorectal cancers, we investigated its effects on HeLa,SW-48, and MRC-5 cell lines. Cell lines were exposed to various concentrations of patulin (i.e., 0.5, 1, 2, and 4 µM), then using methyl thiazolyl tetrazolium (MTT) and bromo-2′-deoxyuridine (BrdU) assays, the rates of apoptosis and cell viability were determined.
Results: The obtained results showed a significant reduction in cell viability and apoptosis induction in a dose-dependent manner. Among all the cell lines, the highest growth inhibition rate was obtained at the 4 μM concentration of patulin.Conclusion: Our results suggested that patulin could significantly decrease tumor growth in human cervical and colorectal cancer models.
- انتشار مقاله: 18-04-1398
- نویسندگان: Mahdi Abastabar,Abolfazl Akbari,Javad Akhtari,Mohammad Taghi Hedayati,Tahereh Shokohi,Hasan Mehrad-Majd,Hosseein Ghalehnoei,Sahar Ghasemi
- مشاهده
- جایگاه : پژوهشی
- مجله: Asian Pacific Journal of Cancer Prevention
- نوع مقاله: Journal Article
- کلمات کلیدی: Diagnosis,Prognosis,Survival,long non-coding RNA,PCAT-1
- چکیده:
- چکیده انگلیسی: Long non-coding RNA (lncRNA) prostate cancer associated transcript 1 (PCAT-1) has been identified as a potential
biomarker for the diagnosis and prognosis of various cancers. We performed this systematic review and meta-analysis
to evaluate the role of dysregulation as well as the biological and clinical significance of lnc-PCAT-1 for predicting the
malignancy status in several cancers. Two independent reviewers conducted an extensive search in electronic databases
of Medline, Embase, Scopus, Web of Science and PubMed until the December of 2017. Five articles investigating the
clinical significance of lncRNA PCAT-1, including 996 patients, were analyzed. Our results revealed that the increased
PCAT-1 expression was related to overall survival (OS) (HR = 1.9, 95%CI: 1.13-3.18, P=0.015). Also, pooled results
of the diagnostic data analysis demonstrated that PCAT-1 has a sensitivity of 0.59 and specificity of 0.66 for cancer
diagnosis. Moreover, pooled area under curve was 0.62 (95% CI: 058–0.69). This meta-analysis revealed that lncRNA
PCAT-1 could be served as a potential diagnostic and prognostic biomarker in various solid tumors.- انتشار مقاله: 13-12-1396
- نویسندگان: Atefeh Talebi,Abolfazl Akbari,Gholam Reza Mobini,Sara Ashtari,Mohamad Amin Pourhoseingholi
- مشاهده
- جایگاه : پژوهشی
- مجله: Asian Pacific Journal of Cancer Prevention
- نوع مقاله: Journal Article
- کلمات کلیدی: Colorectal cancer,CD34,Homeodomain protein TGIF2LX,Ki-67,Transforming growth factor-beta (TGF-β)
- چکیده:
- چکیده انگلیسی:
Background: TGIF2LX (transforming growth factor beta-induced factor 2 like, X-linked) is a homeodomain (HD) protein that has been implicated in the negative regulation of cell signaling pathways. The aim of this study was to investigate the possible functions of TGIF2LX in colon adenocarcinoma cells. Methods: The human SW48 cell line was transfected with cDNA for the wild-type TGIF2LX gene and gene/protein over-expression was confirmed by microscopic analysis, real time RT-PCR and Western blotting techniques. In vitro cell proliferation was evaluated by MTT and BrdU assays. After developing a colon tumor model in nude mice, immunohistochemical (IHC) staining of tumor tissue was carried out for Ki-67 (proliferation) and CD34 (angiogenesis) markers. To predict potential protein partners of TGIF2LX, in-silico analysis was also conducted. Results: Obtained results showed over-expression of TGIF2LX as a potential transcription factor could inhibit either proliferation or angiogenesis (P<0.05) in colon tumors. In-silico results predicted interaction of TGIF2LX with other proteins considered important for cellular development. Conclusions: Our findings provided evidence of molecular mechanisms by which TGIF2LX could act as a tumor suppressor in colon adenocarcinoma cells. Thus, this gene may potentially be a promising option for colon cancer gene-based therapeutic strategies.- انتشار مقاله: 23-11-1395
- نویسندگان: Abolfazl Akbari,Shahram Agah,Mansour Heidari,Gholam Reza Mobini,Ebrahim Faghihloo,Arash Sarveazad,Alireza Mirzaei
- مشاهده