scholarly journals Advances in Research on the Protective Mechanisms of Traditional Chinese Medicine (TCM) in Islet β Cells

2019 ◽  
Vol 2019 ◽  
pp. 1-8 ◽  
Author(s):  
Na Li ◽  
Hongli Zhang ◽  
Xiaohua Li
Keyword(s):  
Chinese Medicine ◽  
Cell Function ◽  
Animal Experiments ◽  
Cell Protection ◽  
Insulin Synthesis ◽  
Treatment Of Diabetes ◽  
Insulinoma Cells

The dysfunction and decreased number of islet β cells are central to the main pathogenesis of diabetes. Improving islet β cell function and increasing the number of β cells are effective approaches to treat diabetes and constitute the main direction of diabetes drug development. The role of Chinese medicine in the treatment of diabetes began to be recognized. In recent years, Chinese medicine monomers have been found to increase insulin synthesis and secretion, reduce β cell-apoptosis, and protect the function of β cells. The results of in vivo animal experiments and in vitro studies on insulinoma cells also suggested TCMs could promote the proliferation of pancreatic islet β cells and induce other cells differentiation or transdifferentiation to islet β cells. Thereby, they may play a role in the treatment of diabetes. In this paper, we will review islet β cell protection with TCMs and the related mechanisms found in recent studies. An in-depth explanation of the role of TCM in islet β cell protection can provide a theoretical basis and research ideas for the development of TCM-based diabetes treatment drugs.

scholarly journals Yanghe Huayan decoction inhibits the capability of trans-endothelium and angiogenesis of HER2+ breast cancer via pAkt signaling

2019 ◽  
Vol 39 (2) ◽  
Author(s):  
Xiao-Fei Liu ◽  
Jing-Wei Li ◽  
Hong-Zhi Chen ◽  
Zi-Yuan Sun ◽  
Guang-Xi Shi ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Chinese Medicine ◽  
Precancerous Lesion ◽  
Tumor Development ◽  
Akt Activation ◽  
Her2 Breast Cancer ◽  
Prevention And Treatment

Abstract Background: Yanghe Huayan Decoction (YHD), a traditional Chinese medicine, is one of the most common complementary medicine currently used in the treatment of breast cancer (BC). It has been recently linked to suppress precancerous lesion and tumor development. The current study sought to explore the role of YHD on trans-endothelium and angiogenesis of BC. Methods: HER2+ BC cells were treated with YHD, Trastuzumab, or the combination in vitro and in vivo to compare the effects of them on trans-endothelium and angiogenesis features. The present study also investigated the potential molecular mechanism of YHD in inhibiting angiogenesis of BC. Results: YHD significantly suppressed the invasion and angiogenesis of BC cells via elevated pAkt signaling. Administration of YHD in vivo also strikingly repressed angiogenesis in tumor grafts. Conclusion: YHD could partially inhibit and reverse tumorigenesis of BC. It also could inhibit Akt activation and angiogenesis in vitro and in vivo. Its effect was superior to trastuzumab. Thus it was suitable for prevention and treatment of BC.

scholarly journals The P2Y6 Receptor Stimulates Bone Resorption by Osteoclasts

Endocrinology ◽  
2011 ◽  
Vol 152 (10) ◽  
pp. 3706-3716 ◽  
Author(s):  
Isabel R. Orriss ◽  
Ning Wang ◽  
Geoffrey Burnstock ◽  
Timothy R. Arnett ◽  
Alison Gartland ◽  
...  
Keyword(s):  
Cell Function ◽  
Bone Cell ◽  
Extracellular Nucleotides ◽  
P2y6 Receptor ◽  
Tomographic Analysis ◽  
G Protein Coupled ◽  
Resorptive Activity

Accumulating evidence indicates that extracellular nucleotides, signaling through P2 receptors, play a significant role in bone remodeling. Osteoclasts (the bone-resorbing cell) and osteoblasts (the bone-forming cell) display expression of the G protein-coupled P2Y6 receptor, but the role of this receptor in modulating cell function is unclear. Here, we demonstrate that extracellular UDP, acting via P2Y6 receptors, stimulates the formation of osteoclasts from precursor cells, while also enhancing the resorptive activity of mature osteoclasts. Furthermore, osteoclasts derived from P2Y6 receptor-deficient (P2Y6R−/−) animals displayed defective function in vitro. Using dual energy x-ray absorptiometry scanning and microcomputed tomographic analysis we showed that P2Y6R−/− mice have increased bone mineral content, cortical bone volume, and cortical thickness in the long bones and spine, whereas trabecular bone parameters were unaffected. Histomorphometric analysis showed the perimeter of the bone occupied by osteoclasts on the endocortical and trabecular surfaces was decreased in P2Y6R−/− mice. Taken together these results show the P2Y6 receptor may play an important role in the regulation of bone cell function in vivo.

scholarly journals The Role of AMPK/mTOR Signaling Pathway in Anticancer Activity of Metformin

2021 ◽  
pp. 501-508
Author(s):  
Nikola Chomanicova ◽  
Andrea Gazova ◽  
Adriana Adamickova ◽  
Simona Valaskova ◽  
Jan Kyselovic
Keyword(s):  
Anticancer Activity ◽  
Mammalian Target Of Rapamycin ◽  
Adenosine Monophosphate ◽  
Mtor Pathway ◽  
Diabetic Patients ◽  
Beneficial Effects ◽  
Treatment Of Diabetes

Metformin (MTF) is a widely used drug for the treatment of diabetes mellitus type 2 (DM2) and frequently used as an adjuvant therapy for polycystic ovarian syndrome, metabolic syndrome, and in some cases also tuberculosis. Its protective effect on the cardiovascular system has also been described. Recently, MTF was subjected to various analyzes and studies that showed its beneficial effects in cancer treatment such as reducing cancer cell proliferation, reducing tumor growth, inducing apoptosis, reducing cancer risk in diabetic patients, or reducing likelihood of relapse. One of the MTF’s mechanisms of action is the activation of adenosine-monophosphate-activated protein kinase (AMPK). Several studies have shown that AMPK/mammalian target of rapamycin (mTOR) pathway has anticancer effect in vivo and in vitro. The aim of this review is to present the anticancer activity of MTF highlighting the importance of the AMPK/mTOR pathway in the cancer process.

scholarly journals LINC00467 Promotes Tumor Progression via Regulation of the NF-kb Signal Axis in Bladder Cancer

2021 ◽  
Vol 11 ◽  
Author(s):  
Jiawei Xiao ◽  
Lian Gong ◽  
Mengqing Xiao ◽  
Dong He ◽  
Liang Xiang ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Signaling Pathway ◽  
Molecular Mechanisms ◽  
Animal Experiments ◽  
Bioinformatic Analysis ◽  
New Strategy ◽  
Patient Prognosis

PurposeLong non-coding RNAs (lncRNAs) play an important role in the occurrence and development of bladder cancer, but the underlying molecular mechanisms remain largely unknown. In this study, we found that LINC00467 was significantly highly expressed in bladder cancer through bioinformatic analysis. The present study aimed to explore the role of LINC00467 in bladder cancer and its possible underlying molecular mechanisms.MethodsThe expression of LINC00467 was obtained from GEO (GSE31189), the TCGA database, and qRT-PCR. The role of LINC00467 in bladder cancer was assessed both in vitro and in vivo. RIP, RNA pulldown, and CO-IP were used to demonstrate the potential mechanism by which LINC00467 regulates the progression of bladder cancer.ResultsThrough the analysis of GEO (GSE133624) and the TCGA database, it was found that LINC00467 was highly expressed in bladder cancer tissues and that the expression of LINC00467 was significantly negatively correlated with patient prognosis. Cell and animal experiments suggest that LINC00467 promotes the proliferation and invasion of bladder cancer cells. On the one hand, LINC00467 can directly bind to NF-kb-p65 mRNA to stabilize its expression. On the other hand, LINC00467 can directly bind to NF-kb-p65 to promote its translocation into the nucleus to activate the NF-κB signaling pathway, which promotes the progression of bladder cancer.ConclusionsLINC00467 is highly expressed in bladder cancer and can promote the progression of bladder cancer by regulating the NF-κB signaling pathway. Therefore, targeting LINC00467 is very likely to provide a new strategy for the treatment of bladder cancer and for improving patient prognosis.

scholarly journals The Role of Methionine Aminopeptidase 2 in Lymphangiogenesis

2020 ◽  
Vol 21 (14) ◽  
pp. 5148
Author(s):  
Rawnaq Esa ◽  
Eliana Steinberg ◽  
Dvir Dror ◽  
Ouri Schwob ◽  
Mehrdad Khajavi ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Cell Function ◽  
Loss Of Function ◽  
Methionine Aminopeptidase ◽  
Zebrafish Model ◽  
Lymphatic Capillary ◽  
Intracellular Enzyme

During the metastasis process, tumor cells invade the blood circulatory system directly from venous capillaries or indirectly via lymphatic vessels. Understanding the relative contribution of each pathway and identifying the molecular targets that affect both processes is critical for reducing cancer spread. Methionine aminopeptidase 2 (MetAp2) is an intracellular enzyme known to modulate angiogenesis. In this study, we investigated the additional role of MetAp2 in lymphangiogenesis. A histological staining of tumors from human breast-cancer donors was performed in order to detect the level and the localization of MetAp2 and lymphatic capillaries. The basal enzymatic level and activity in vascular and lymphatic endothelial cells were compared, followed by loss of function studies determining the role of MetAp2 in lymphangiogenesis in vitro and in vivo. The results from the histological analyses of the tumor tissues revealed a high MetAp2 expression, with detectable sites of co-localization with lymphatic capillaries. We showed slightly reduced levels of the MetAp2 enzyme and MetAp2 mRNA expression and activity in primary lymphatic cells when compared to the vascular endothelial cells. The genetic and biochemical manipulation of MetAp2 confirmed the dual activity of the enzyme in both vascular and lymphatic remodulation in cell function assays and in a zebrafish model. We found that cancer-related lymphangiogenesis is inhibited in murine models following MetAp2 inhibition treatment. Taken together, our study provides an indication that MetAp2 is a significant contributor to lymphangiogenesis and carries a dual role in both vascular and lymphatic capillary formation. Our data suggests that MetAp2 inhibitors can be effectively used as anti-metastatic broad-spectrum drugs.

scholarly journals An overview on the interplay between nutraceuticals and gut microbiota

PeerJ ◽  
2018 ◽  
Vol 6 ◽  
pp. e4465 ◽  
Author(s):  
Adrian Catinean ◽  
Maria Adriana Neag ◽  
Dana Maria Muntean ◽  
Ioana Corina Bocsan ◽  
Anca Dana Buzoianu
Keyword(s):  
Health Status ◽  
Side Effects ◽  
Alternative Therapy ◽  
Animal Experiments ◽  
Health Benefits ◽  
Health Benefit ◽  
Synthetic Drugs

BackgroundNowadays, growing attention was being given to the alternative ways to prevent or treat diseases. Nutraceuticals are used increasingly for this purpose. Many of these are being used as alternative therapy. Classic therapy with synthetic drugs, although very effective, has many side effects. The term “nutraceuticals” refers to the link between the nutritional and pharmaceutical domains. Also, lately, many studies have been done to investigate the role of microbiota in maintaining health. There is the hypothesis that some of the health benefits of nutraceuticals are due to their ability to change the microbiota. The aim of this review was to emphasize the link between the most commonly used nutraceuticals, the microbiota and the health benefits.MethodsWe selected the articles in PubMed, published up to July 2017, that provided information about most used nutraceuticals, microbiota and health benefits. In this review, we incorporate evidence from various types of studies, including observational,in vitroandin vivo, clinical studies or animal experiments.ResultsThe results demonstrate that many nutraceuticals change the composition of microbiota and can interfere with health status of the patients.DiscussionThere is evidence which sustains the importance of nutraceuticals in people’s health through microbiota but further studies are needed to complete the assessment of nutraceuticals in health benefit as a consequence of microbiota’s changing.

scholarly journals Leukotrienes modulate secretion of progesterone and prostaglandins during the estrous cycle and early pregnancy in cattle: an in vivo study

Reproduction ◽  
2010 ◽  
Vol 140 (5) ◽  
pp. 767-776 ◽  
Author(s):  
Anna J Korzekwa ◽  
Mamadou M Bah ◽  
Andrzej Kurzynowski ◽  
Karolina Lukasik ◽  
Agnieszka Groblewska ◽  
...  
Keyword(s):  
Mrna Expression ◽  
Estrous Cycle ◽  
Early Pregnancy ◽  
Luteal Phase ◽  
Reproductive Tract ◽  
Cell Function ◽  
Ovarian Cell

Recently, we showed that leukotrienes (LTs) regulate ovarian cell functionin vitro. The aim of this study was to examine the role of LTs in corpus luteum (CL) function during both the estrous cycle and early pregnancyin vivo. mRNA expression of LT receptors (BLTfor LTB4andCYSLTfor LTC4), and 5-lipoxygenase (5-LO) in CL tissue and their localization in the ovary were studied during the estrous cycle and early pregnancy. Moreover, concentrations of LTs (LTB4and C4) in the CL tissue and blood were measured.5-LOandBLTmRNA expression increased on days 16–18 of the cycle, whereasCYSLTmRNA expression increased on days 16–18 of the pregnancy. The level of LTB4was evaluated during pregnancy compared with the level of LTC4, which increased during CL regression. LT antagonists influenced the duration of the estrous cycle: the LTC4antagonist (azelastine) prolonged the luteal phase, whereas the LTB4antagonist (dapsone) caused earlier luteolysisin vivo. Dapsone decreased progesterone (P4) secretion and azelastine increased P4secretion during the estrous cycle. In summary, LT action in the bovine reproductive tract is dependent on LT type: LTB4is luteotropic during the estrous cycle and supports early pregnancy, whereas LTC4is luteolytic, regarded as undesirable in early pregnancy. LTs are produced/secreted in the CL tissue, influence prostaglandin function, and serve as important factors during the estrous cycle and early pregnancy in cattle.

scholarly journals Clinical Trial andIn VitroStudy for the Role of Cartilage and Synovia in Acute Articular Infection

2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Elia R. Langenmair ◽  
Eva J. Kubosch ◽  
Gian M. Salzmann ◽  
Samuel Beck ◽  
Hagen Schmal
Keyword(s):  
Clinical Trial ◽  
Cell Function ◽  
Joint Infection ◽  
Synovial Fibroblasts ◽  
Joint Infections ◽  
Anti Inflammatory

Objective. Osteoarthritis is a long-term complication of acute articular infections. However, the roles of cartilage and synovia in this process are not yet fully understood.Methods. Patients with acute joint infections were enrolled in a prospective clinical trial and the cytokine composition of effusions compared in patients with arthroplasty (n= 8) or with intact joints (n= 67). Cytokines and cell function were also analyzed using a humanin vitromodel of joint infection.Results. Synovial IL-1βlevels were significantly higher in patients with arthroplasty (p= 0.004). Higher IL-1βconcentrations were also found in thein vitromodel without chondrocytes (p< 0.05). The anti-inflammatory cytokines IL-4 and IL-10 were consistently expressedin vivoandin vitro, showing no association with the presence of cartilage or chondrocytes. In contrast, FasL levels increased steadilyin vitro, reaching higher levels without chondrocytes (p< 0.05). Likewise, the viability of synovial fibroblasts (SFB) during infection was higher in the presence of chondrocytes. The cartilage-metabolism markers aggrecan and bFGF were at higher concentrations in intact joints, but also synthesized by SFB.Conclusions. Our data suggest an anti-inflammatory effect of cartilage associated with the SFBs’ increased resistance to infections, which displayed the ability to effectively synthesize cartilage metabolites.The trial is registered with DRKS00003536, MISSinG.

scholarly journals The role of G-protein-coupled membrane estrogen receptor in mouse Leydig cell function—in vivo and in vitro evaluation

2018 ◽  
Vol 374 (2) ◽  
pp. 389-412 ◽  
Author(s):  
M. Kotula-Balak ◽  
P. Pawlicki ◽  
A. Milon ◽  
W. Tworzydlo ◽  
M. Sekula ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
G Protein ◽  
Leydig Cell ◽  
Cell Function ◽  
G Protein Coupled ◽  
Mouse Leydig Cell ◽  
Leydig Cell Function

scholarly journals The role of H-2-linked genes in helper T-cell function. III. Expression of immune response genes for trinitrophenyl conjugates of poly-L(Tyr, Glu)-poly-D,L-Ala--poly-L-Lys in B cells and macrophages.

1978 ◽  
Vol 147 (6) ◽  
pp. 1596-1610 ◽  
Author(s):  
P Marrack ◽  
J W Kappler
Keyword(s):  
T Cells ◽  
B Cells ◽  
Cell Function ◽  
Cell Types ◽  
High Responder ◽  
In Vitro Response ◽  
Low Responder

Using lymph node T cells from poly-L(Tyr,Glu)-poly-D,L-Ala--poly-L-Lys[(TG)-A--L]-primed animals and B cells from animals primed with trinitrophenylated (TNP) protein or lipopolysaccharide, we have obtained anti-TNP-(TG)-A--L direct plaque-forming responses in vitro. Response to this antigen was shown to be controlled by the H-2 haplotype of the animal studied. The strain distribution of in vitro response was very similar to that previously reported by others for in vivo secondary IgG responses to (TG)-A--L. We investigated the cell types expressing the Ir gene(s) for (TG)-A--L in our cultures. F1, high responder x low responder mice were primed with (TG)-A--L. Their T cells were active in stimulating anti-TNP-(TG)-A--L responses of high responder but not low responder B cells and macrophages (MPHI), even though both preparations of B cells and Mphi were obtained from mice congenic at H-2 with one of the parents of the F1. For three low responder strains tested, of the H-2h2, H-2k, and H-2f haplotypes, the anti-TNP-(TG)-A--L response of low responder B cells and Mphis in the presence of high responder, F1 T cells could not be improved by the addition of high responder, antigen-bearing Mphis to the cultures. In one strain of the H-2a haplotype, it was shown that neither the B cells nor Mphis could be functional in anti-TNP-(TG)-A--L responses. Our results therefore suggested the Ir genes for anti-TNP-(TG)-A--L responses were expressed at least in B cells in all the low responder strains we studied, and, in mice of the H-2a haplotype, in Mphis too.

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