scholarly journals Cytoprotective Effect of Eriodictyol in UV-irradiated Keratinocytes via Phosphatase-dependent Modulation of both the p38 MAPK and Akt Signaling Pathways

2011 ◽  
Vol 27 (5) ◽  
pp. 513-524 ◽  
Author(s):  
Eung-Ryoung Lee ◽  
Jung-Hyun Kim ◽  
Hye Yeon Choi ◽  
Kilsoo Jeon ◽  
Ssang-Goo Cho
Keyword(s):  
Signaling Pathways ◽  
P38 Mapk ◽  
Akt Signaling ◽  
Cytoprotective Effect

scholarly journals TGF-β1 targets Smad, p38 MAPK, and PI3K/Akt signaling pathways to induce PFKFB3 gene expression and glycolysis in glioblastoma cells

FEBS Journal ◽  
2017 ◽  
Vol 284 (20) ◽  
pp. 3437-3454 ◽  
Author(s):  
Ana Rodríguez-García ◽  
Paula Samsó ◽  
Pere Fontova ◽  
Helga Simon-Molas ◽  
Anna Manzano ◽  
...  
Keyword(s):  
Gene Expression ◽  
Signaling Pathways ◽  
P38 Mapk ◽  
Akt Signaling ◽  
Glioblastoma Cells ◽  
Tgf Β1

Paricalcitol pretreatment attenuates renal ischemia/reperfusion injury by inhibiting p38 MAPK and activating PI3K/Akt signaling pathways

2019 ◽  
Vol 44 (4) ◽  
pp. 452-461
Author(s):  
Zahide Cavdar ◽  
Cemre Ural ◽  
Ayse Kocak ◽  
Sevki Arslan ◽  
Sibel Ersan ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
P38 Mapk ◽  
Caspase 3 ◽  
Ischemia Reperfusion ◽  
Akt Signaling ◽  
Albino Rats ◽  
Sod Activity ◽  
Interstitial Inflammation ◽  
Tnf Α ◽  
Active Caspase

Abstract Objective This study aimed to investigate the renoprotective effects of paricalcitol, a synhetic vitamin D analog, through its possible roles on p38 MAPK and PI3K/Akt signaling pathways to prevent oxidative stress, inflammation and apoptosis during renal I/R. Materials and methods Total 20 kidney tissues of sham (n = 6), subjected to renal I/R bilaterally for 45 min ischemia followed by 24 h reperfusion (n = 7) and paricalcitol (0.3 μg/kg, ip) pretreated Wistar albino rats (n =7) were used in this study. Interstitial inflammation and active caspase-3 expression were evaluated histologically. TNF-α, IL-1β, kidney injury molecule-1 (KIM-1), MDA and SOD activity in kidneys were analysed biochemically. Furthermore, activation of p38 MAPK, PI3K/Akt signaling pathways and NFκB p65 were evaluated by western blot. Results Paricalcitol pretreatment significantly reduced interstitial inflammation during renal I/R, which was consistent with decreased tumor TNF-α, IL-1β, active caspase-3 and KIM-1 expression. Paricalcitol also reduced MDA level and attenuated the reduction of SOD activity in the kidney during I/R. Moreover, paricalcitol could suppress the p38 MAPK and NFκB p65, and also activate PI3K/Akt signaling pathway during renal I/R. Conclusion All these findings indicate that paricalcitol may be an effective practical strategy to prevent renal I/R injury.

Chondroprotective effects of glucosamine involving the p38 MAPK and Akt signaling pathways

2008 ◽  
Vol 28 (10) ◽  
pp. 1009-1016 ◽  
Author(s):  
Yi-Cheng Lin ◽  
Yu-Chih Liang ◽  
Ming-Thau Sheu ◽  
Yu-Chen Lin ◽  
Ming-Shium Hsieh ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
P38 Mapk ◽  
Akt Signaling

scholarly journals The Ameliorating Effect of Plasma Protein from Tachypleus tridentatus on Cyclophosphamide-Induced Acute Kidney Injury in Mice

Marine Drugs ◽  
2019 ◽  
Vol 17 (4) ◽  
pp. 227 ◽  
Author(s):  
Xinhuang Kang ◽  
Mengyao Jing ◽  
Guoguang Zhang ◽  
Lanzheng He ◽  
Pengzhi Hong ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Signaling Pathways ◽  
P38 Mapk ◽  
Plasma Protein ◽  
Renal Cell ◽  
Molecular Mechanisms ◽  
Kidney Injury ◽  
Akt Signaling ◽  
Growth Effect ◽  
Tachypleus Tridentatus

In the study, the protective effect of plasma protein from Tachypleus tridentatus (PPTT) on acute kidney injury (AKI) and the related molecular mechanisms were first investigated by Western blotting analyses, TdT-mediated dUTP Nick-End Labeling (TUNEL) assay, and immunohistochemistry. It was found that PPTT had an obviously inhibitory effect on Reactive oxygen species (ROS) in cyclophosphamide (CTX)-exposed mice. Furthermore, results demonstrated that the renal cell death mode is due to inducing apoptosis and autophagy inhibited by dose-dependent PPTT in mice treated with CTX by decreasing the protein expression of bax, beclin-1, and LC3 and increasing the expression of bcl-2. Moreover, the p38 MAPK and PI3K/Akt signaling pathways were observed to take part in the PPTT-induced renal cell growth effect by enhancing the upregulation of the expression of Akt and p-Akt as well as the downregulation of the expression of p38 and p-p38, which indicated a PPTT ameliorating effect on AKI CTX-induced in mice through p38 MAPK and PI3K/Akt signaling pathways. Briefly, this article preliminarily studies the mechanism of the PPTT ameliorating effect on AKI CTX-induced in mice, which helps to provide a reference for PPTT clinical application in AKI therapy.

scholarly journals X-ray Irradiation Inhibits Inflammation and Glial Scar Formation through p38 MAPK and Akt Signaling Pathways and Promotes the Recovery of Nerve Function after Spinal Cord Injury in Rats

2021 ◽  
Author(s):  
Yi Wang ◽  
Yanping Niu ◽  
Fanguo Lin ◽  
Peng Su ◽  
Liesong Chen ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Signaling Pathways ◽  
P38 Mapk ◽  
Akt Signaling ◽  
Glial Scar ◽  
Scar Formation ◽  
Nerve Function ◽  
X Ray ◽  
Cord Injury

Abstract Spinal cord injury (SCI) is a common clinical disease that can cause permanent disruption of nerve function. Inflammation and glial scar formation influence the recovery of injured spinal cord. X-ray irradiation can reduce inflammation, inhibit cell proliferation and increase cell apoptosis. However, the regulatory effects of X-ray irradiation on inflammation and glial scars and the underlying molecular mechanisms are still unclear. This study aimed to explore the effect of X-ray irradiation on the progression of SCI. Behavioural experiments show that X-ray irradiation can effectively improve the motor function of SCI rats. X-ray irradiation inhibits the inflammatory response by reducing the expression of inflammatory factors (including TNF-α and IL-1β) at the lesion site, thereby enhancing the survival of neuronal cells .X-ray irradiation effectively inhibited the formation of the glial scar (the expression of the related proteins GFAP and vimentin) in the lesion. In addition, the p38 MAPK and Akt signaling pathways were activated after SCI in rats, but these signaling pathways were significantly blocked after X-ray irradiation. Furthermore, the 10 Gy dose had the most significant effects among the 2 Gy, 10 Gy and 20 Gy doses. In summary, X-ray irradiation can inhibit inflammation and glial scar formation by blocking the p38 MAPK and Akt signaling pathways, thereby improving the recovery of nerve function in rats with SCI. Therefore, X-ray irradiation provides a new strategy for the treatment of SCI.

scholarly journals Sargassum serratifolium Extract Attenuates Interleukin-1β-Induced Oxidative Stress and Inflammatory Response in Chondrocytes by Suppressing the Activation of NF-κB, p38 MAPK, and PI3K/Akt

2018 ◽  
Vol 19 (8) ◽  
pp. 2308 ◽  
Author(s):  
Cheol Park ◽  
Jin-Woo Jeong ◽  
Dae-Sung Lee ◽  
Mi-Jin Yim ◽  
Jeong Lee ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
P38 Mapk ◽  
Articular Chondrocytes ◽  
Umbilical Vein ◽  
Akt Signaling ◽  
Mitogen Activated Protein Kinase ◽  
Interleukin 1Β ◽  
Joint Disease ◽  
Sargassum Serratifolium ◽  
Anti Inflammatory

Osteoarthritis (OA) is a degenerative joint disease that is characterized by irreversible articular cartilage destruction by inflammatory reaction. Among inflammatory stimuli, interleukin-1β (IL-1β) is known to play a crucial role in OA pathogenesis by stimulating several mediators that contribute to cartilage degradation. Recently, the marine brown alga Sargassum serratifolium has been reported to exhibit antioxidant and anti-inflammatory effects in microglial and human umbilical vein endothelial cell models using lipopolysaccharide and tumor necrosis factor-α, but its beneficial effects on OA have not been investigated. This study aimed to evaluate the anti-osteoarthritic effects of ethanol extract of S. serratifolium (EESS) in SW1353 human chondrocytes and, in parallel, primary rat articular chondrocytes. Our results showed that EESS effectively blocked the generation of reactive oxygen species in IL-1β-treated SW1353 and rat primary chondrocytes, indicating that EESS has a potent antioxidant activity. EESS also attenuated IL-1β-induced production of nitric oxide (NO) and prostaglandin E2, major inflammatory mediators in these cells, which was associated with the inhibition of inducible NO synthase and cyclooxygenase-2 expression. Moreover, EESS downregulated the level of gene expression of matrix metalloproteinase (MMP)-1, -3 and -13 in SW1353 chondrocytes treated with IL-1β, resulting in their extracellular secretion reduction. In addition, the IL-1β-induced activation of nuclear factor-kappa B (NF-κB) was restored by EESS. Furthermore, EESS reduced the activation of p38 mitogen-activated protein kinase (MAPK) and phosphatidylinositol-3-kinase (PI3K)/Akt signaling pathways upon IL-1β stimulation. These results indicate that EESS has the potential to exhibit antioxidant and anti-inflammatory effects through inactivation of the NF-κB, p38 MAPK, and PI3K/Akt signaling pathways. Collectively, these findings demonstrate that EESS may have the potential for chondroprotection, and extracts of S. serratifolium could potentially be used in the prevention and treatment of OA.

scholarly journals IL-1β Promotes Vasculogenic Mimicry of Breast Cancer Cells Through p38/MAPK and PI3K/Akt Signaling Pathways

2021 ◽  
Vol 11 ◽  
Author(s):  
Muhammad Azhar Nisar ◽  
Qin Zheng ◽  
Muhammad Zubair Saleem ◽  
Bulbul Ahmmed ◽  
Muhammad Noman Ramzan ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Signaling Pathways ◽  
P38 Mapk ◽  
Breast Cancer Cells ◽  
Vasculogenic Mimicry ◽  
Akt Signaling ◽  
Immunofluorescent Staining ◽  
Morphological Evidence ◽  
Mcf 7

Vasculogenic mimicry (VM), a micro vessel-like structure formed by the cancer cells, plays a pivotal role in cancer malignancy and progression. Interleukin-1 beta (IL-1β) is an active pro-inflammatory cytokine and elevated in many tumor types, including breast cancer. However, the effect of IL-1β on the VM of breast cancer has not been clearly elucidated. In this study, breast cancer cells (MCF-7 and MDA-MB-231) were used to study the effect of IL-1β on the changes that can promote VM. The evidence for VM stimulated by IL-1β was acquired by analyzing the expression of VM-associated biomarkers (VE-cadherin, VEGFR-1, MMP-9, MMP-2, c-Fos, and c-Jun) via western blot, immunofluorescent staining, and Immunohistochemistry (IHC). Additionally, morphological evidence was collected via Matrigel-based cord formation assay under normoxic/hypoxic conditions and microvessel examination through Hematoxylin and Eosin staining (H&E). Furthermore, the STRING and Gene Ontology database was also used to analyze the VM-associated interacting molecules stimulated by IL-β. The results showed that the expression of VM biomarkers was increased in both MCF-7 and MDA-MB-231 cells after IL-1β treatment. The increase in VM response was observed in IL-1β treated cells under both normoxia and hypoxia. IL-1β also increased the activation of transcription factor AP-1 complex (c-Fos/c-Jun). The bioinformatics data indicated that p38/MAPK and PI3K/Akt signaling pathways were involved in the IL-1β stimulation. It was further confirmed by the downregulated expression of VM biomarkers and reduced formation of the intersections upon the addition of the signaling pathway inhibitors. The study suggests that IL-1β stimulates the VM and its associated events in breast cancer cells via p38/MAPK and PI3K/Akt signaling pathways. Aiming the VM-associated molecular targets promoted by IL-1β may offer a novel anti-angiogenic therapeutic strategy to control the aggressiveness of breast cancer cells.

Biological role of AKT, and regulation of AKT signaling pathway by thymoquinone: perspectives in cancer therapeutics

2020 ◽  
Vol 20 ◽  
Author(s):  
Md. Junaid ◽  
Yeasmin Akter ◽  
Syeda Samira Afrose ◽  
Mousumi Tania ◽  
Md. Asaduzzaman Khan
Keyword(s):  
Clinical Trials ◽  
Signaling Pathways ◽  
Signaling Pathway ◽  
Inhibitory Effect ◽  
Akt Signaling ◽  
Review Article ◽  
Therapeutic Drug ◽  
Akt Signaling Pathway ◽  
Anti Cancer

Background: AKT/PKB is an important enzyme with numerous biological functions, and its overexpression is related to the carcinogenesis. AKT stimulates different signaling pathways that are downstream of activated tyrosine kinases and phosphatidylinositol 3-kinase, hence functions as an important target for anti-cancer drugs. Objective: In this review article, we have interpreted the role of AKT signaling pathways in cancer and natural inhibitory effect of Thymoquinone (TQ) in AKT and its possible mechanism. Method: We have collected the updated information and data on AKT, their role in cancer and inhibitory effect of TQ in AKT signaling pathway from google scholar, PubMed, Web of Science, Elsevier, Scopus and many more. Results: There are many drugs already developed, which can target AKT, but very few among them have passed clinical trials. TQ is a natural compound, mainly found in black cumin, which has been found to have potential anti-cancer activities. TQ targets numerous signaling pathways, including AKT, in different cancers. In fact, many studies revealed that AKT is one of the major targets of TQ. The preclinical success of TQ suggests its clinical studies on cancer. Conclusion: This review article summarizes the role of AKT in carcinogenesis, its potent inhibitors in clinical trials, and how TQ acts as an inhibitor of AKT and TQ’s future as a cancer therapeutic drug.

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