scholarly journals Chondroprotective Activity ofMurraya exoticathrough Inhibitingβ-Catenin Signaling Pathway

2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Longhuo Wu ◽  
Haiqing Liu ◽  
Rui Zhang ◽  
Linfu Li ◽  
Jialin Li ◽  
...  
Keyword(s):  
Degenerative Joint Disease ◽  
Joint Disease ◽  
Chondrocyte Apoptosis ◽  
Dependent Manner ◽  
Chain Reaction ◽  
Protein Expressions ◽  
Murraya Exotica ◽  
Oa Chondrocytes ◽  
Polymerase Chain ◽  
Dose Dependent

Osteoarthritis (OA) is a degenerative joint disease that affects millions of people. Currently, there is no effective drug treatment for it. The purpose of this study is to investigate the chondroprotective effects ofMurraya exotica(L.) on OA. The rat OA models were duplicated to prepare for separating OA chondrocytes, synovial fluid (SF), and serum containingM. exotica(50 mg/kg, 100 mg/kg, and 200 mg/kg),M. exoticashowed the activity of decreasing the contents of TNF-αand IL-1βin SF and the chondrocyte apoptosis in a dose-dependent manner. To investigate the probable mechanism, quantitative real-time polymerase chain reaction (qRT-PCR) and western blotting were used to determine gene expression and protein profiles, respectively. The results reveal thatM. exoticacan downregulate mRNA and protein expressions ofβ-catenin and COX-2 and reporter activity significantly. Conclusively,M. exoticaexhibits antiapoptotic chondroprotective activity probably through inhibitingβ-catenin signaling.

scholarly journals Palmatine attenuates isoproterenol-induced pathological hypertrophy via selectively inhibiting HDAC2 in rats

2017 ◽  
Vol 30 (4) ◽  
pp. 406-412 ◽  
Author(s):  
Yonggang Yuan ◽  
Wanzhong Peng ◽  
Yongxing Liu ◽  
Zesheng Xu
Keyword(s):  
Therapeutic Potential ◽  
Dependent Manner ◽  
Chain Reaction ◽  
Protein Levels ◽  
Downstream Effector ◽  
Effector Genes ◽  
Therapeutic Value ◽  
Pathological Hypertrophy ◽  
Polymerase Chain ◽  
Dose Dependent

This study aimed to exploit the potential therapeutic value of palmatine in treatment of cardiac hypertrophy and the underlying molecular mechanism. Rat hypertrophy model was established by intraperitoneal isoproterenol (ISO) injection. The hypertrophy was evaluated with cardiac hypertrophic parameters, hemodynamic parameters, lipid profile, and non-specific cardiac markers. The animals were intraperitoneally administrated with either palmatine or vehicle. The relative expressions of ANP, BNP, HDAC2, HDAC5, KLF4, and INPP5F transcripts were determined by real-time polymerase chain reaction (PCR). The relative protein levels of HDAC2, HDAC5, KLF4, and INPP5F were analyzed by immunoblotting. Palmatine treatment significantly attenuated ISO-induced hypertrophy in rats and elicited remarkable repressions in ANP, BNP, and HDAC2 transcriptions but not HDAC5. The downstream effector genes KLF4 and INPP5F were greatly restored in a dose-dependent manner in response to palmatine treatment. Our data demonstrated that palmatine possessed promising therapeutic potential against hypertrophy, which was mediated by modulation of HDAC2-KLF4/INPP5F pathway.

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.

scholarly journals Kahweol Exerts Skin Moisturizing Activities by Upregulating STAT1 Activity

2021 ◽  
Vol 22 (16) ◽  
pp. 8864
Author(s):  
Hongxi Chen ◽  
Mohammad Amjad Hossain ◽  
Jong-Hoon Kim ◽  
Jae Youl Cho
Keyword(s):  
Proper Time ◽  
Radical Scavenging ◽  
Polymerase Chain Reaction Analysis ◽  
Luciferase Assay ◽  
Dependent Manner ◽  
Diphenyltetrazolium Bromide ◽  
Polymerase Chain ◽  
Radical Scavenging Ability ◽  
The Relationship ◽  
Dose Dependent

Kahweol is a diterpene present in coffee. Until now, several studies have shown that kahweol has anti-inflammatory and anti-angiogenic functions. Due to the limited research available about skin protection, this study aims to discern the potential abilities of kahweol and the possible regulation targets. First, the cytotoxicity of kahweol was checked by 3-4-5-dimethylthiazol-2-yl)-2-5-diphenyltetrazolium bromide assay, while 2,20-azino-bis (3ethylbenzothiazoline-6-sulphonic acid) diammonium salt and 1-diphenyl-2-picryl-hydrazyl were used to examine the radical scavenging ability. Polymerase chain reaction analysis was performed to explore the proper time points and doses affecting skin hydration and barrier-related genes. Luciferase assay and Western blotting were used to explore the possible transcription factors. Finally, fludarabine (a STAT1 inhibitor) was chosen to discern the relationship between skin-moisturizing factors and STAT1. We found that HaCaT cells experienced no toxicity from kahweol, and kahweol displayed moderate radical scavenging ability. Moreover, kahweol increased the outcome of HAS1, HAS2, occludin, and TGM-1 from six hours in a dose-dependent manner as well as the activation of STAT1 from six hours. Additionally, kahweol recovered the suppression of HAS2, STAT1-mediated luciferase activity, and HA secretion, which was all downregulated by fludarabine. In this study, we demonstrated that kahweol promotes skin-moisturizing activities by upregulating STAT1.

scholarly journals Blocking of checkpoint receptor PD-L1 aggravates osteoarthritis in macrophage-dependent manner in the mice model

2019 ◽  
Vol 33 ◽  
pp. 205873841882076 ◽  
Author(s):  
Shenghou Liu ◽  
Jiqiang Mi ◽  
Wenguang Liu ◽  
Shipeng Xiao ◽  
Chunzheng Gao
Keyword(s):  
Inflammatory Cytokine ◽  
Cruciate Ligament ◽  
Mrna Level ◽  
Degenerative Joint Disease ◽  
Joint Disease ◽  
Enzyme Linked Immunosorbent Assay ◽  
Dependent Manner ◽  
Mice Model ◽  
Safranin O ◽  
Factor Α

As a chronic degenerative joint disease, osteoarthritis is among the most common diseases all over the world. In osteoarthritis, inflammation plays an important role in the generation of joint symptoms and the development of disease. When the programmed cell death-1 (PD-1)/programmed death-ligand 1 (PD-L1) immune checkpoint is blocked, the antitumor immunity will be enhanced. We aim to illustrate the function of PD-L1 in osteoarthritis. Osteoarthritis in mice was induced by the injection of collagenase or anterior cruciate ligament transection (ACLT). Anti-PD-L1 was employed to block the signal of PD-L1. Knee joints histological sections were stained by Safranin-O. The level of cytokine was checked by enzyme-linked immunosorbent assay (ELISA) and mRNA level was shown by quantitative reverse transcriptase polymerase chain reaction. The blockade of PD-L1 signal up-regulated inflammatory response and promoted the development of osteoarthritis in mice. The inflammatory cytokine interleukin-6 and tumor necrosis factor-α expression were promoted by PD-L1 blocking in macrophages. Osteoarthritis was aggravated when the expression of inflammatory cytokine is elevated in macrophages. Our results indicated that the blockade of PD-L1 signal in macrophages elevates the expression of inflammatory cytokine and promotes the development of osteoarthritis in mice, which could be utilized as a potential diagnostic and therapeutic target for osteoarthritis patients.

scholarly journals Bax Targeted by miR-29a Regulates Chondrocyte Apoptosis in Osteoarthritis

2019 ◽  
Vol 2019 ◽  
pp. 1-9 ◽  
Author(s):  
Guiqiang Miao ◽  
Xuehui Zang ◽  
Huige Hou ◽  
Hui Sun ◽  
Lihui Wang ◽  
...  
Keyword(s):  
Cartilage Degeneration ◽  
Degenerative Joint Disease ◽  
Joint Disease ◽  
Luciferase Reporter ◽  
Chondrocyte Apoptosis ◽  
Reporter Assay ◽  
Proapoptotic Protein ◽  
Regulation Mechanisms ◽  
Direct Target

Osteoarthritis (OA) is a chronic degenerative joint disease, where chondrocyte apoptosis is responsible for cartilage degeneration. Bax is a well-known proapoptotic protein of the Bcl-2 family, involved in a large number of physiological and pathological processes. However, the regulation mechanisms of Bax underlying chondrocyte apoptosis in OA remain unknown. In the present study, we determined the role of Bax in human OA and chondrocyte apoptosis. The results showed that Bax was upregulated in chondrocytes from the articular cartilage of OA patients and in cultured chondrocyte-like ATDC5 cells treated by IL-1β. Bax was identified to be the direct target of miR-29a by luciferase reporter assay and by western blotting. Inhibition of miR-29a by the mimics protested and overexpression by miR-29a inhibitors aggravated ATDC5 apoptosis induced by IL-1β. These data reveal that miR-29a/Bax axis plays an important role in regulating chondrocyte apoptosis and suggest that targeting the proapoptotic protein Bax and increasing expression levels of miR-29a emerge as potential approach for protection against the development of OA.

scholarly journals The Role of Estrogens in Rheumatoid Arthritis Physiopathology

2020 ◽  
Author(s):  
Maria Fernanda Romo-García ◽  
Martín Zapata-Zuñiga ◽  
José Antonio Enciso-Moreno ◽  
Julio Enrique Castañeda-Delgado
Keyword(s):  
Rheumatoid Arthritis ◽  
Direct Action ◽  
Hormone Replacement ◽  
Joint Disease ◽  
Dependent Manner ◽  
Sexual Hormones ◽  
Dose Dependent ◽  
Estrogen Administration

Rheumatoid arthritis (RA) is a chronic, inflammatory joint disease that can lead to irreversible disability. It affects women in a higher proportion than men (3:1 cases). Several reports suggest a link between female sexual hormones (estrogens) and RA features. It’s been described that biological processes where basal estrogen levels are altered like in menstruation, pregnancy, and menopause modifies RA onset, flare, disease severity, and inflammation. Estrogens have a direct action upon the immune system though ERα and ERβ receptors, which have distinct affinity to estrogen concentrations and modifications and have effects upon RA in a dose and receptor dependent manner. The studies focused on dose dependent response at experimental settings reveal a wide (from 25 pg/L to several μg/L) and even contradictory spectrum of effects in patients and cells. This chapter summarizes the contributions and effects of estrogens in RA physiopathology, clinical features, and discusses the possible contributions of estrogen administration and concentration of hormone replacement therapy (HRT) to improve the quality of life and reduce the symptoms of RA patients based on the knowledge of the biology of these hormones.

Benzodiazepines Block α2-Containing Inhibitory Glycine Receptors in Embryonic Mouse Hippocampal Neurons

2003 ◽  
Vol 90 (1) ◽  
pp. 89-99 ◽  
Author(s):  
Liu Lin Thio ◽  
Ananth Shanmugam ◽  
Keith Isenberg ◽  
Kelvin Yamada
Keyword(s):  
Hippocampal Neurons ◽  
Clinical Effects ◽  
Dependent Manner ◽  
Glycine Receptors ◽  
Binding Studies ◽  
Chloride Currents ◽  
Embryonic Mouse ◽  
Voltage Dependent ◽  
Polymerase Chain ◽  
Dose Dependent

Inhibitory glycine receptors (GlyRs) in the mammalian cortex probably contribute to brain development and to maintaining tonic inhibition. Given their presence throughout the cortex, their modulation likely has important physiological consequences. Although benzodiazepines potentiate γ-aminobutyric acidA receptors (GABAARs), they may also modulate GlyRs because binding studies initially suggested that they act at GlyRs. Furthermore, their diminished ability to potentiate neonatal GABAARs suggests that they may exert their beneficial clinical effects at another site in the developing brain. Therefore we examined the effect of benzodiazepines on whole cell currents mediated by GlyRs in cultured embryonic mouse hippocampal neurons. First, we determined the GlyR subunit composition in this preparation. Glycine, β-alanine, and taurine activate strychnine-sensitive chloride currents in a dose-dependent manner. Maximal concentrations of the three agonists produce equal, nonadditive responses as expected of full agonists. The pharmacological properties of the GlyR currents including their pattern of modulation by picrotoxinin, picrotin, and tropisetron indicate that GlyRs consist of α2β heteromers and α2 homomers. Reverse transcriptase polymerase chain reaction (RTPCR) studies confirmed the presence of α2 and β subunits. Second, we found that micromolar concentrations of some benzodiazepines, including chlordiazepoxide and nitrazepam, inhibit GlyR currents. Nitrazepam inhibition of GlyRs is noncompetitive, is not voltage dependent, and does not reflect enhanced desensitization. Thus benzodiazepines allosterically inhibit α2-containing GlyRs in embryonic mouse hippocampal neurons via a “low”-affinity site.

Chondroitin - application in the treatment of degenerative joint disease

2016 ◽  
Vol 18 (6) ◽  
pp. 621-628 ◽  
Author(s):  
Wiesław Tomaszewski
Keyword(s):  
Molecular Level ◽  
Proteolytic Enzymes ◽  
Chondroitin Sulphate ◽  
Cartilage Degradation ◽  
Degenerative Joint Disease ◽  
Joint Disease ◽  
Chondrocyte Apoptosis ◽  
Structural Elements ◽  
Acid Biosynthesis ◽  
Physiological Processes

Chondroitin is an organic compound, belonging to the group of glycosaminoglycans. In the treatment of degenerative joint disease, aka osteoarthritis, chondroitin sulphate is applied as a medicine or a dietary supplement. The biological importance of chondroitin sulphate has been already largely determined. The newest data on glycobiology research suggest that proteoglycans, as well as their complex polysaccharide macroparticles not only are the structural elements, but also they participate in multiple metabolic processes at a molecular level as well as in the physiological processes, regulating this type of mechanisms. The preparations applied in the treatment of degenerative joint disease, containing chondroitin sulphate, are attributed numerous therapeutic and chondroprotective properties including stabilizing synthesis processes and cartilage degradation through stimulation and inhibition of chondrocyte apoptosis (production of the elements of the intracellular substance and osteocyte stimulation), an increased proteoglycan and hyaluronic acid biosynthesis, inhibition of the activity of proteolytic enzymes and hyaluronidase, reduction of inflammatory mediators (prostaglandins and leukotrienes) and a decreased collagen II degradation. Based on the results of the multidirectional research available in the newest source literature, the analysis of the therapeutic efficacy and safety of chondroitin application in the treatment of degenerative joint disease was conducted.

scholarly journals The Study of HLA-G Gene and Protein Expression in Patients withRecurrent Miscarriage

2019 ◽  
Vol 9 (1) ◽  
pp. 70-75 ◽  
Author(s):  
Elnaz Mosaferi ◽  
Nazila Alizadeh Gharamaleki ◽  
Laya Farzadi ◽  
Jafar Majidi ◽  
Zohreh Babaloo ◽  
...  
Keyword(s):  
Gene Expression ◽  
Polymerase Chain Reaction ◽  
Protein Expression ◽  
Sample Size ◽  
G Protein ◽  
Recurrent Miscarriage ◽  
Chain Reaction ◽  
Gene And Protein Expression ◽  
Protein Expressions ◽  
Polymerase Chain

Purpose: Although it has been frequently confirmed that HLA-G plays an important role in thereproduction and pregnancy, the pattern of HLA-G gene and its protein expression are rarelyaddressed in studies. Therefore we conducted this study in regard to evaluate the HLA-G geneand its protein expression in the women’s placenta with recurrent miscarriage.Methods: Placental samples were obtained from the women who were admitted for deliveryor abortion in Al Zahra and Taleghani hospitals, Tabriz, Iran. HLA-G gene expression wasdetermined by real-time polymerase chain reaction (PCR) and HLA-G protein expression wasassessed by western blotting and immunofluorescence staining in the tissue samples.Results: The results showed a significant decrease in the expression of gene and proteins ofHLA-G in the women with recurrent miscarriage compared to the control placental tissues.Conclusion: According to the obtained results, it was concluded that the decrement of HLA-Ggene and protein expressions are associated with recurrent miscarriage. Since there areconflicting results from other studies, it is suggested to conduct a more comprehensive similarstudy with greater sample size.

Thrombopoietin in thrombocytopenic mice: evidence against regulation at the mRNA level and for a direct regulatory role of platelets

Blood ◽  
1996 ◽  
Vol 87 (2) ◽  
pp. 567-573 ◽  
Author(s):  
R Stoffel ◽  
A Wiestner ◽  
RC Skoda
Keyword(s):  
Mrna Level ◽  
Rnase Protection Assay ◽  
Chain Reaction ◽  
Rnase Protection ◽  
Dose Dependent Fashion ◽  
Liver And Kidney ◽  
Polymerase Chain ◽  
Dose Dependent ◽  
Posttranscriptional Level

Thrombopoietin (TPO), originally described as an activity in the serum of thrombocytopenic animals that leads to increased production of platelets, has recently been isolated and cloned. Its closest relative in the cytokine superfamily, erythropoietin (EPO), is transcriptionally regulated during anemia, and it was expected that TPO would similarly be regulated during thrombocytopenia. We induced thrombocytopenia in mice and confirmed that TPO activity was upregulated, as determined by a bioassay. Liver and kidney were found to be the major sources of TPO mRNA. Surprisingly, TPO mRNA in these tissues was not upregulated in thrombocytopenic mice. Using a sensitive RNase protection assay that can distinguish between TPO isoforms, we found no change in the profile of mRNA for these isoforms. A semiquantitative reverse transcription- polymerase chain reaction assay also did not demonstrate upregulation of TPO mRNA in the spleen. Thus, the increase of TPO activity during thrombocytopenia is not caused by regulation at the level of TPO mRNA. Furthermore, isolated mouse platelets absorbed high amounts of bioactive TPO out of TPO-conditioned medium in a dose-dependent fashion. Our results are consistent with TPO protein being regulated at a posttranscriptional level and/or directly through absorption and metabolism by platelets.

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