Characterization of polysaccharide from longan pulp as the macrophage stimulator

RSC Advances ◽  
2015 ◽  
Vol 5 (118) ◽  
pp. 97163-97170 ◽  
Author(s):  
Yang Yi ◽  
Hongxun Wang ◽  
Ruifen Zhang ◽  
Ting Min ◽  
Fei Huang ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
P38 Mapk ◽  
Macrophage Activation

A 44.7-kDa polysaccharide LPIIa from longan pulp was mainly composed of →6)-Glc-(1→, →5)-Ara-(1→, →4)-Man-(1→ and →6)-Gal-(1→. It stimulated macrophage activation partlyviaTLR4 and TLR2, followed by p38 MAPK- and NF-κB-dependent signaling pathways.

Chemical characterization of a novel polysaccharide ASKP-1 from Artemisia sphaerocephala Krasch seed and its macrophage activation via MAPK, PI3k/Akt and NF-κB signaling pathways in RAW264.7 cells

2017 ◽  
Vol 8 (3) ◽  
pp. 1299-1312 ◽  
Author(s):  
Daoyuan Ren ◽  
Dehui Lin ◽  
Aamina Alim ◽  
Quan Zheng ◽  
Xingbin Yang
Keyword(s):  
Signaling Pathways ◽  
Molecular Mechanism ◽  
Macrophage Activation ◽  
Chemical Characterization ◽  
Immunomodulatory Effect ◽  
Raw264.7 Cells ◽  
Raw264.7 Macrophages ◽  
Artemisia Sphaerocephala

The aim of this study was to investigate the molecular mechanism underlying the immunomodulatory effect of the purified Artemisia sphaerocephala Krasch seed polysaccharide (ASKP-1) in RAW264.7 macrophages.

MALAT1 as a Versatile Regulator of Cancer: Overview of the updates from Predatory role as Competitive Endogenous RNA to Mechanistic In-sights

2020 ◽  
Vol 20 ◽  
Author(s):  
Ammad Ahmad Farooqi ◽  
Evangelia Legaki ◽  
Maria Gazouli ◽  
Silvia Rinaldi ◽  
Rossana Berardi
Keyword(s):  
Molecular Biology ◽  
Detailed Analysis ◽  
Signaling Pathways ◽  
Individualized Medicine ◽  
Signaling Cascades ◽  
Oncogenic Signaling ◽  
Non Coding Rnas ◽  
Oncogenic Signaling Pathways ◽  
Competitive Endogenous Rna

: Central dogma of molecular biology has remained cornerstone of classical molecular biology but serendipitous discovery of microRNAs (miRNAs) in nematodes paradigmatically shifted our current understanding of the intricate mech-anisms which occur during transitions from transcription to translation. Discovery of miRNA captured tremendous attention and appreciation and we had witnessed an explosion in the field of non-coding RNAs. Ground-breaking discoveries in the field of non-coding RNAs have helped in better characterization of microRNAs and long non-coding RNAs (LncRNAs). There is an ever-increasing list of miRNA targets which are regulated by MALAT1 to stimulate or repress expression of tar-get genes. However, in this review our main focus is to summarize mechanistic insights related to MALAT1-mediated regu-lation of oncogenic signaling pathways. We have discussed how MALAT1 modulated TGF/SMAD and Hippo pathways in various cancers. We have also comprehensively summarized how JAK/STAT and Wnt/β-catenin pathways stimulated MALAT1 expression and consequentially how MALAT1 potentiated these signaling cascades to promote cancer. MALAT1 research has undergone substantial broadening however, there is still a need to identify additional mechanisms. MALAT1 is involved in multi-layered regulation of multiple transduction cascades and detailed analysis of different pathways will be helpful in getting a step closer to individualized medicine.

The Impact of Royal Jelly against Hepatic Ischemia/Reperfusion-Induced Hepatocyte Damage in Rats: The Role of Cytoglobin, Nrf-2/HO-1/COX-4, and P38-MAPK/NF-κB-p65/TNF-α Signaling Pathways

2020 ◽  
Vol 14 (1) ◽  
pp. 88-100
Author(s):  
Fares E.M. Ali ◽  
Heba M. Saad Eldien ◽  
Nashwa A.M. Mostafa ◽  
Abdulrahman H. Almaeen ◽  
Mohamed R.A. Marzouk ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
P38 Mapk ◽  
Royal Jelly ◽  
Ischemia Reperfusion ◽  
Histopathological Changes ◽  
Down Regulation ◽  
Hepatic Ischemia ◽  
Tnf Α ◽  
Hepatic Ischemia Reperfusion ◽  
The Impact

Objective: The present study was conducted to elucidate the underlying molecular mechanism as well as the potential hepatoprotective effects of royal jelly (RJ) against hepatic ischemia/reperfusion (IR) injury. Methods: Rats were assigned into four groups; sham (received vehicle), IR (30 minutes ischemia and 45 minutes reperfusion), sham pretreated with RJ (200 mg/kg P.O.), and IR pretreated with RJ (200 mg/kg P.O.). The experiment has lasted for 28 days. Results: Hepatic IR significantly induced hepatic dysfunctions, as manifested by elevation of serum transaminases, ALP and LDH levels. Moreover, hepatic IR caused a significant up-regulation of P38-MAPK, NF-κB-p65, TNF-α and MDA levels along with marked down-regulation of Nrf-2, HO-1, COX-4, cytoglobin, IκBa, IL-10, GSH, GST and SOD levels. Additionally, marked histopathological changes were observed after hepatic IR injury. On the contrary, pretreatment with RJ significantly improved hepatic functions along with the alleviation of histopathological changes. Moreover, RJ restored oxidant/antioxidant balance as well as hepatic expressions of Nrf-2, HO-1, COX-4, and cytoglobin. Simultaneously, RJ significantly mitigated the inflammatory response by down-regulation of P38-MAPK, NF-κB-p65, TNF-α expression. Conclusion: The present results revealed that RJ has successfully protected the liver against hepatic IR injury through modulation of cytoglobin, Nrf-2/HO-1/COX-4, and P38-MAPK/NF-κB-p65/TNF-α signaling pathways.

scholarly journals Molecular Pathogenesis of Hodgkin Lymphoma: Past, Present, Future

2020 ◽  
Vol 21 (18) ◽  
pp. 6623 ◽  
Author(s):  
Marc Bienz ◽  
Salima Ramdani ◽  
Hans Knecht
Keyword(s):  
Immune System ◽  
Targeted Therapy ◽  
Signaling Pathways ◽  
Hodgkin Lymphoma ◽  
Genetic Instability ◽  
Host Immune System ◽  
Cellular Interactions ◽  
Classical Hodgkin Lymphoma ◽  
The Past

Our understanding of the tumorigenesis of classical Hodgkin lymphoma (cHL) and the formation of Reed–Sternberg cells (RS-cells) has evolved drastically in the last decades. More recently, a better characterization of the signaling pathways and the cellular interactions at play have paved the way for new targeted therapy in the hopes of improving outcomes. However, important gaps in knowledge remain that may hold the key for significant changes of paradigm in this lymphoma. Here, we discuss the past, present, and future of cHL, and review in detail the more recent discoveries pertaining to genetic instability, anti-apoptotic signaling pathways, the tumoral microenvironment, and host-immune system evasion in cHL.

Trans-ferulic acid ameliorates cisplatin-induced testicular damage via suppression of TLR4, P38-MAPK, and ERK1/2 signaling pathways

2021 ◽  
Author(s):  
Emad H. M. Hassanein ◽  
Basel A. Abdel-Wahab ◽  
Fares E. M. Ali ◽  
Omnia A. M. Abd El-Ghafar ◽  
Magy R. Kozman ◽  
...  
Keyword(s):  
Ferulic Acid ◽  
Signaling Pathways ◽  
P38 Mapk ◽  
Testicular Damage

scholarly journals Lipopolysaccharide activates innate immune responses in murine intestinal myofibroblasts through multiple signaling pathways

2009 ◽  
Vol 296 (3) ◽  
pp. G601-G611 ◽  
Author(s):  
Kristen L. W. Walton ◽  
Lisa Holt ◽  
R. Balfour Sartor
Keyword(s):  
Immune Responses ◽  
Signaling Pathways ◽  
P38 Mapk ◽  
Western Blotting ◽  
Pi3 Kinase ◽  
Innate Immune ◽  
Innate Immune Responses ◽  
Fold Induction ◽  
Cox 2 ◽  
Multiple Signaling

Myofibroblasts (MF) play an important role in intestinal wound healing. A compromised epithelial barrier exposes intestinal subepithelial MF to luminal bacterial products. However, responses of murine intestinal MF to bacterial adjuvants and potential roles of intestinal MF in innate immune responses are not well defined. Our aims in this study were to determine innate immune responses and intracellular signaling pathways of intestinal MF exposed to LPS, a prototypic Toll-like receptor (TLR) ligand. Expression of TLR4 in primary murine intestinal MF cultures was confirmed by RT-PCR and Western blotting. LPS-induced secretion of prostaglandin E2 (PGE2), interleukin (IL)-6, and keratinocyte-derived chemokines (KC) was measured by ELISA. Intracellular responses to LPS were assessed by Western blotting for NF-κB p65, Iκ-Bα, Akt, p38 MAP kinase, and cyclooxygenase-2 (COX-2). LPS induced rapid phosphorylation of NF-κB p65, Akt, and p38 MAPK and degradation of Iκ-Bα. LPS induced expression of COX-2 and secretion of PGE2 (2.0 ± 0.8-fold induction vs. unstimulated cells), IL-6 (6.6 ± 0.4-fold induction), and KC (12.5 ± 0.4-fold induction). Inhibition of phosphoinositide-3 (PI3)-kinase, p38 MAPK, or NF-κB pathways reduced LPS-induced PGE2, IL-6, and KC secretion. These studies show that primary murine intestinal MF respond to LPS, evidenced by activation of NF-κB, PI3-kinase, and MAPK signaling pathways and secretion of proinflammatory molecules. Inhibition of these pathways attenuated LPS-dependent PGE2, IL-6, and KC production, indicating that LPS activates MF by multiple signaling pathways. These data support the hypothesis that MF are a component of the innate immune system and may exert paracrine effects on adjacent epithelial and immune cells by responding to luminal bacterial adjuvants.

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