scholarly journals Burn Ointment Promotes Cutaneous Wound Healing by Modulating the PI3K/AKT/mTOR Signaling Pathway

2021 ◽  
Vol 12 ◽  
Author(s):  
Dali Gan ◽  
Qiyuan Su ◽  
Hanwen Su ◽  
Li Wu ◽  
Jun Chen ◽  
...  
Keyword(s):  
Wound Healing ◽  
Signaling Pathway ◽  
High Performance ◽  
Scientific Evidence ◽  
Latency Period ◽  
Analgesic Efficacy ◽  
Mtor Signaling ◽  
Mtor Signaling Pathway ◽  
Hot Plate ◽  
Anti Inflammatory

Burn ointment (BO) is a clinically useful medicine for the treatment of burns and scalds. However, there is no enough scientific evidence to report the effect of BO on wound healing and its analgesic and anti-inflammatory efficacy. The aim of this work was to evaluate the anti-inflammatory and analgesic efficacy of BO and to reveal the potential wound healing properties and related mechanisms of BO. In this work, the content of active ingredients of BO was determined by high-performance liquid chromatography (HPLC). Two animal models of inflammation were used to study its anti-inflammatory activity, and a hot plate method was used to evaluate its analgesic effect. In addition, mouse incision and rat burn models were used to investigate the effect of BO on the anti-inflammatory and wound healing mechanisms. The results showed that BO was safe for topical application, and BO could significantly inhibit auricular swelling in mice and paw swelling in rats and significantly prolong the latency period of paw licking in the hot plate experiment in mice. It can also accelerate wound healing and repair scars by promoting the formation of new epithelial tissues in rat burn models. In addition, BO significantly downregulated the serum level of TNF-α and significantly increased the serum levels of VEGF and TGF-β1. Also, BO promoted the expression of collagen I and increased the ratio in p-PI3K/PI3K, p-AKT/AKT, and p-mTOR/mTOR pathways. Our results demonstrate the safety and efficacy of BO and suggest that activation of the PI3K/AKT/mTOR signaling pathway may play an important role in the promotion of wound healing by BO.

Acemannan accelerates cell proliferation and skin wound healing through AKT/mTOR signaling pathway

2015 ◽  
Vol 79 (2) ◽  
pp. 101-109 ◽  
Author(s):  
Wei Xing ◽  
Wei Guo ◽  
Cun-Hua Zou ◽  
Ting-Ting Fu ◽  
Xiang-Yun Li ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Wound Healing ◽  
Signaling Pathway ◽  
Skin Wound ◽  
Mtor Signaling ◽  
Mtor Signaling Pathway ◽  
Skin Wound Healing

scholarly journals MicroRNA-99 Family Targets AKT/mTOR Signaling Pathway in Dermal Wound Healing

PLoS ONE ◽  
2013 ◽  
Vol 8 (5) ◽  
pp. e64434 ◽  
Author(s):  
Yi Jin ◽  
Stéphanie D. Tymen ◽  
Dan Chen ◽  
Zong Juan Fang ◽  
Yan Zhao ◽  
...  
Keyword(s):  
Wound Healing ◽  
Signaling Pathway ◽  
Mtor Signaling ◽  
Mtor Signaling Pathway ◽  
Dermal Wound Healing ◽  
Dermal Wound

scholarly journals Hyperin Alleviates Triptolide-Induced Ovarian Granulosa Cell Injury by Regulating AKT/TSC1/mTORC1 Signaling

2021 ◽  
Vol 2021 ◽  
pp. 1-13
Author(s):  
Fang You ◽  
Junyan Cao ◽  
Li Cheng ◽  
Xiaogu Liu ◽  
Li Zeng
Keyword(s):  
Signaling Pathway ◽  
Granulosa Cell ◽  
High Performance ◽  
Cell Injury ◽  
Ovarian Function ◽  
Interaction Network ◽  
Mtor Signaling ◽  
Network Pharmacology ◽  
Mtor Signaling Pathway ◽  
Mtorc1 Signaling

Premature ovarian insufficiency (POI) is characterized by the loss of ovarian function before 40 years of age and affects approximately 1% of women worldwide. Caragana sinica is a traditional Miao (a Chinese ethnic minority) medicine that improves ovarian function and follicular development. In the present study, we aimed to investigate the effect of active ingredients of C. sinica on POI and determine underlying mechanisms. Herein, the chemical composition of the C. sinica compound was analyzed using ultra-high-performance liquid chromatography, which identified hyperin (HR) as one of the main ingredients in C. sinica. Then, interaction targets of HR and POI were predicted and analyzed using network pharmacology and bioinformatics. The effect of HR on triptolide (TP)-induced granulosa cell injury was evaluated, and the underlying mechanism was explored based on bioinformatic results. A total of 100 interaction targets for POI and HR were obtained. The protein-protein interaction network of identified interaction targets emphasized the topological importance of AKT1. Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis revealed that HR might regulate POI by modulating the mechanistic target of rapamycin (mTOR) signaling pathway. In addition, the KEGG graph of the mTOR signaling pathway revealed that AKT phosphorylation inhibits the TSC1/2, while TSC1/2 activation inhibits the expression of mTORC1. The fundamental experiment revealed that HR increased proliferation, progesterone receptor levels, and estradiol levels decreased by TP in KGN cells. Additionally, HR alleviated TP-induced apoptosis and G1/G1 phase arrest in KGN cells. Western blotting demonstrated that HR increased the phosphorylation of AKT and mTORC1 and decreased TSC1 expression in TP-induced KGN cells. Collectively, our findings revealed that HR alleviates TP-induced granulosa cell injury by regulating AKT/TSC1/mTORC1 signaling, providing insight into the treatment of POI.

scholarly journals Time-Dependent Changes in Hepatic Sphingolipid Accumulation and PI3K/Akt/mTOR Signaling Pathway in a Rat Model of NAFLD

2021 ◽  
Vol 22 (22) ◽  
pp. 12478
Author(s):  
Klaudia Sztolsztener ◽  
Karolina Konstantynowicz-Nowicka ◽  
Ewa Harasim-Symbor ◽  
Adrian Chabowski
Keyword(s):  
Signaling Pathway ◽  
High Performance ◽  
Glucose Transporter ◽  
Significant Inhibition ◽  
Mtor Signaling ◽  
Time Dependent ◽  
Standard Diet ◽  
Mtor Signaling Pathway ◽  
Akt Phosphorylation ◽  
Male Wistar Rats

Increased lipid bioavailability in a diet favors lipid accumulation, enhancing hepatic lipotoxicity and contributing to insulin resistance (IR) development. The aim of our study was to examine time-dependent alterations in the intrahepatic content of sphingolipids and insulin signaling pathway in rats fed a high-fat diet (HFD). The experiment was conducted on male Wistar rats receiving a standard diet or HFD for five weeks. At the end of each experimental feeding week, liver sphingolipids were determined using high-performance liquid chromatography. The expression of proteins from the sphingolipid pathway and glucose transporter expression were assessed by Western blot. The content of phosphorylated form of proteins from the insulin pathway was detected by a multiplex assay kit. Our results revealed that HFD enhanced hepatic ceramide deposition by increasing the expression of selected proteins from sphingomyelin and salvage pathways in the last two weeks. Importantly, we observed a significant inhibition of Akt phosphorylation in the first week of HFD and stimulation of PTEN and mTOR phosphorylation at the end of HFD. These changes worsened the PI3K/Akt/mTOR signaling pathway. We may postulate that HFD-induced reduction in the insulin action in the time-dependent matter was exerted by excessive accumulation of sphingosine and sphinganine rather than ceramide.

Triptolide exhibits anti-inflammatory effects on adipocytes and macrophages by inhibition of AMPK/mTOR pathway

2021 ◽  
Author(s):  
Xue-li Li ◽  
Zhao Liu
Keyword(s):  
Signaling Pathway ◽  
Therapeutic Potential ◽  
Chinese Herb ◽  
Mtor Signaling ◽  
Low Grade ◽  
Mtor Signaling Pathway ◽  
Raw264.7 Macrophages ◽  
Inflammatory Models ◽  
Tnf Α ◽  
Anti Inflammatory

Abstract Obesity is a growing global health problem and chronic over-nutrition disease with lipid accumulation that results in low-grade chronic inflammation in the microenvironment of adipose tissue. Triptolide is a diterpene lactone compound extracted from the roots of the Chinese herb TWHF and possesses a therapeutic potential due to its immunosuppressive and anti-inflammatory properties. In this study, we built obesity-related inflammatory models of adipocytes using LPS, Ma-CM and raw264.7 macrophages, while the obesity-related inflammatory models of macrophages were built using LPS and Ad-CM system. We used these inflammatory models to investigate the anti-inflammatory property of triptolide. Treatment of triptolide (0.005, 0.010, 0.020 and 0.040 μ M) inhibited LPS-induced or macrophages conditioned medium-stimulated activation of AMPK/mTOR signaling pathway (p < 0.05). The results showed that triptolide reduced the release of chemokines MCP-1, RANTES, EOTAXIN and KC in LPS, Ma-CM or RAW264.7 macrophages-stimulated 3T3-L1 adipocytes. Triptolide also diminished MCP-1, RANTES, EOTAXIN, KC and TNF-α in Ad-CM stimulated RAW264.7 macrophages, while expression of MCP-1, RANTES, TNF-α, GM-CSF and IL-6 was decreased in LPS stimulated RAW264.7 macrophages (p < 0.05). These results demonstrate that triptolide is not only effective against inflammatory response of RAW264.7 macrophages or 3T3-L1 adipocytes, but also disrupts the crosstalk between macrophages and adipocytes, particularly by inhibiting secretion of pro-inflammatory mediators through inhibiting the activation of AMPK/mTOR signaling pathway. Triptolide might benefit to ameliorate obesity-induced inflammatory diseases.

scholarly journals Ozone oil promotes wound healing by increasing the migration of fibroblasts via PI3K/Akt/mTOR signaling pathway

2017 ◽  
Vol 37 (6) ◽  
Author(s):  
Weirong Xiao ◽  
Hua Tang ◽  
Meng Wu ◽  
Yangying Liao ◽  
Ke Li ◽  
...  
Keyword(s):  
Wound Healing ◽  
Growth Factor ◽  
Signaling Pathway ◽  
Western Blotting ◽  
Mtor Signaling ◽  
Mtor Signaling Pathway ◽  
Skin Injury ◽  
Mesenchymal Transition ◽  
Fibroblast Migration ◽  
Western Blotting Assay

Skin injury affects millions of people via the uncontrolled inflammation and infection. Many cellular components including fibroblasts and signaling pathways such as transforming growth factor-β (TGF-β) were activated to facilitate the wound healing to repair injured tissues. C57BL/6 female mice were divided into control and ozone oil treated groups. Excisional wounds were made on the dorsal skin and the fibroblasts were isolated from granulation tissues. The skin injured mouse model revealed that ozone oil could significantly decrease the wound area and accelerate wound healing compared with control group. QPCR and Western blotting assays showed that ozone oil up-regulated collagen I, α-SMA, and TGF-β1 mRNA and protein levels in fibroblasts. Wound healing assay demonstrated that ozone oil could increase the migration of fibroblasts. Western blotting assay demonstrated that ozone oil increased the epithelial–mesenchymal transition (EMT) process in fibroblasts via up-regulating fibronectin, vimentin, N-cadherin, MMP-2, MMP-9, insulin-like growth factor binding protein (IGFBP)-3, IGFBP5, and IGFBP6, and decreasing epithelial protein E-cadherin and cellular senescence marker p16 expression. Mechanistically, Western blotting assay revealed that ozone oil increased the phosphorylation of PI3K, Akt, and mTOR to regulate the EMT process, while inhibition of PI3K reversed this effect of ozone oil. At last, the results from Cytometric Bead Array (CBA) demonstrated ozone oil significantly decreased the inflammation in fibroblasts. Our results demonstrated that ozone oil facilitated the wound healing via increasing fibroblast migration and EMT process via PI3K/Akt/mTOR signaling pathway in vivo and in vitro. The cellular and molecular mechanisms we found here may provide new therapeutic targets for the treatment of skin injury.

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