Neuroprotective efficacy of nano‐CoQ against propionic acid toxicity in rats: Role of BDNF and CREB protein expressions

2020 ◽  
Vol 34 (4) ◽  
Author(s):  
Ahlam Alhusaini ◽  
Iman H. Hasan ◽  
Bashayer Alrumayyan ◽  
Marwa Alesikri ◽  
Khansa Alanazi ◽  
...  
Keyword(s):  
Propionic Acid ◽  
Creb Protein ◽  
Protein Expressions ◽  
Neuroprotective Efficacy ◽  
Acid Toxicity

scholarly journals Decreased Expression of GPER1 Gene and Protein in Goiter

2015 ◽  
Vol 2015 ◽  
pp. 1-5 ◽  
Author(s):  
Raquel Weber ◽  
Ana Paula Santin Bertoni ◽  
Laura Walter Bessestil ◽  
Ilma Simoni Brum ◽  
Tania Weber Furlanetto
Keyword(s):  
Estrogen Receptor ◽  
Quantitative Polymerase Chain Reaction ◽  
Thyroid Tissue ◽  
Chain Reaction ◽  
Normal Thyroid ◽  
Protein Levels ◽  
Protein Expressions ◽  
Polymerase Chain ◽  
G Protein Coupled

Goiter is more common in women, suggesting that estrogen could be involved in its physiopathology. The presence of classical estrogen receptors (ERαand ERβ) has been described in thyroid tissue, suggesting a direct effect of estrogen on the gland. A nonclassic estrogen receptor, the G-protein-coupled estrogen receptor (GPER1), has been described recently in several tissues. However, in goiter, the presence of this receptor has not been studied yet. We investigated GPER1 gene and protein expressions in normal thyroid and goiter using reverse transcription quantitative polymerase chain reaction (RT-qPCR) and Western blot, respectively. In normal thyroid (n=16) and goiter (n=19), GPER1 gene was expressed in all samples, while GPER1 protein was expressed in all samples of normal thyroid (n=15) but in only 72% of goiter samples (n=13). When comparing GPER1 gene and protein levels in both conditions, gene expression and protein levels were higher in normal thyroid than in goiter, suggesting a role of this receptor in this condition. Further studies are needed to elucidate the role of GPER1 in normal thyroid and goiter.

The Role of Different Molecular Markers in Papillary Thyroid Cancer Patients with Acromegaly

2018 ◽  
Vol 127 (07) ◽  
pp. 437-444 ◽  
Author(s):  
Fatma Ela Keskin ◽  
Hande Mefkure Ozkaya ◽  
Sina Ferahman ◽  
Ozlem Haliloglu ◽  
Adem Karatas ◽  
...  
Keyword(s):  
Thyroid Cancer ◽  
Papillary Thyroid Cancer ◽  
Ex Vivo ◽  
Papillary Thyroid ◽  
Cerrahpasa Medical Faculty ◽  
Protein Expressions ◽  
Galectin 3 ◽  
Benign Nodules ◽  
Igf1 Expression

Abstract Purpose Prevalence of papillary thyroid cancer (PTC) is increased in patients with acromegaly. We aimed to determine the protein expression of BRAF, RAS, RET, insulin like growth factor 1(IGF1), Galectine 3, CD56 in patients with PTC related acromegaly and to compare the extensity of these expressions with normal PTC patients and benign thyroid nodules. Methods We studied 313 patients with acromegaly followed in Cerrahpasa Medical Faculty, Endocrinology and Metabolism Clinic between 1998 and 2015. On the basis of availability of pathological specimen of thyroid tissues, thyroid samples of 13 patients from 19 with acromegaly related PTC (APTC), 20 normal PTC and 20 patients with multinodulary goiter (MNG) were histopathologically evaluated. Protein expressions were determined via immunohistochemical staining in ex-vivo tumor samples and benign nodules. Results The incidence of PTC in acromegaly patients were 6% (n=19). Among patients with PTC, APTC and MNG, all the immunohistochemical protein expressions we have studied were higher in papillary thyroid cancer groups (p<0.01, for all). Between PTC group without acromegaly and APTC, galectin 3 and IGF1 expression was significantly higher in acromegalic patients (p<0.01 for all) while RAS was predominantly higher in PTC patients without acromegaly (p<0.01). Conclusion BRAF expression was not higher in PTC with acromegaly patients compared to PTC patients without acromegaly. Galectine 3 and IGF1 were expressed more intensively in APTC. These positive protein expressions may have more influence on determining malign nodules among acromegaly patients.

Role of Cannabidiol and Tetrahydrocannabivarin on Paclitaxel-Induced Neuropathic Pain in Rodents

2021 ◽  
Author(s):  
Anil Kumar Kalvala ◽  
Arvind Bagde ◽  
Peggy Arthur ◽  
Sunil Kumar Surapaneni ◽  
Ramesh Nimma ◽  
...  
Keyword(s):  
Primary Cultures ◽  
P38 Map Kinase ◽  
Control Group ◽  
Cb1 Receptors ◽  
Neuroprotective Effects ◽  
Sd Rats ◽  
Protein Expressions ◽  
Behavioral Parameters ◽  
Neurobehavioral Symptoms

Abstract The purpose of this study was to investigate the neuroprotective effects of phytocannabinoids, synthetic cannabidiol (CBD) and tetrahydrocannabivarin (THCV) and their combination on taxol induced peripheral neuropathy (PIPN) in mice. Briefly, six groups of C57BL/6J mice (n = 6) were used. PTX (8 mg/kg/day, i.p.) was given to the mice on days 1, 3, 5, and 7 to induce neuropathy. Mice were evaluated for their behavioral parameters and also at the end of the study, DRG collected from the animals were subjected to RNA sequence and westernblot analysis. Further, immunocytochemistry and mitochondrial functional assays were performed on cultured DRGs derived from SD rats. The combination of CBD and THCV improved thermal and mechanical neurobehavioral symptoms in mice by two folds as compared to individual treatments. KEGG (RNA Sequencing) identified P38-MAPK, AMPK, and PI3K-AKT pathways as potential CBD and THCV therapeutic targets. In PTX-treated animals, the expression of p-AMPK, SIRT1, NRF2, HO1, SOD2, and catalase was significantly reduced (p<0.001), whereas the expression of PI3K, p-AKT, p-P38 MAP kinase, BAX, TGF-, NLRP3 inflammasome, and caspase 3 was significantly increased (p<0.001) when compared to control group. In reversing these protein expressions, combination therapy outperformed single therapies. CBD and THCV treatment increased AMPK, Catalase, and Complex I expression while decreasing mitochondrial superoxides in DRG primary cultures. In mice and DRG primary cultures, WAY100135 and rimonabant inhibited the effects of CBD and THCV by blocking 5 HT1A and CB1 receptors. In conclusion, entourage effect of CBD and THCV combination against PIPN appears to protect neurons in mice by modulating 5HT1A and CB1 receptors, respectively.

Beclin 1, LC3, and p62 expression in paraquat-induced pulmonary fibrosis

2019 ◽  
Vol 38 (7) ◽  
pp. 794-802 ◽  
Author(s):  
G Xu ◽  
X Wang ◽  
H Yu ◽  
C Wang ◽  
Y Liu ◽  
...  
Keyword(s):  
Pulmonary Fibrosis ◽  
Light Chain ◽  
Lung Fibrosis ◽  
Beclin 1 ◽  
Related Protein ◽  
Protein Expressions ◽  
Hematoxylin And Eosin ◽  
Hematoxylin And Eosin Staining ◽  
Related Proteins

Paraquat (PQ) is a highly toxic herbicide to humans. Pulmonary fibrosis is one of the most typical features of PQ poisoning, which develops from several days to weeks after ingestion. However, the mechanism of fibrosis is still unclear. In this study, we aimed to determine expressions of autophagy-related markers Beclin 1, microtubule-associated protein light chain 3 (LC3), and p62 in PQ-poisoned lungs and to explore the role of autophagy in pulmonary fibrosis induced by PQ. We detected markers of lung fibrosis and expressions of autophagy-related protein in the specimens from eight fatal cases of PQ poisoning by hematoxylin and eosin staining, Masson’s trichrome staining, and immunohistochemistry. Based on the staining results of lung fibrosis, these cases were divided into two groups, fibrosis and non-fibrosis groups. The correlation between autophagy protein expressions and pulmonary fibrosis was examined. The results demonstrated that the autophagy-related proteins were significantly expressed in fibrosis group compared with the non-fibrosis group. There was a significantly positive correlation between these protein expressions and severity of lung fibrosis. In conclusion, autophagy dysfunction may be involved in lung fibrogenesis caused by PQ poisoning. This may be a promising clue for understanding the molecular mechanism underlying PQ-induced lung fibrosis and provide evidence for treating fibrosis by regulating the level of autophagy.

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