scholarly journals Hair Growth Promotion Effect of Nelumbinis Semen Extract with High Antioxidant Activity

2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Hyeon Ju Park ◽  
Guang-Ri Jin ◽  
Jae Hyun Jung ◽  
Su Bin Hwang ◽  
Su Hyun Lee ◽  
...  
Keyword(s):  
Antioxidant Activity ◽  
Hair Loss ◽  
Hair Growth ◽  
Growth Patterns ◽  
Control Group ◽  
And Migration ◽  
Tgf Β1 ◽  
Proliferation And Migration ◽  
Nelumbinis Semen

This study investigated the hair regeneration promotion and hair loss prevention properties of Nelumbinis Semen (NS) extract in vitro and in vivo. The effect of NS on the proliferation and migration of human dermal papilla cells (hDPCs) was measured in vitro via CCK-8 and scratch migration assays, after which the antioxidant activity of NS was also quantified. NS extracts were then applied to the back of 7-week-old C57BL/6 mice for 3 weeks to monitor hair growth patterns and hair follicle (HF) histology. The mice were divided into three groups: negative control group (NC; DMSO), positive control group (PC; 3% minoxidil), and experimental group (NS extract 1,000 ppm). Moreover, to study the molecular mechanisms by which NS extract regenerates hair growth, real-time PCR was used to analyze factors related to the hair growth cycle. The NS extracts were found to possess high antioxidant properties due to their high flavonoid contents and electron-donating ability. Moreover, NS extracts enhanced hDPC proliferation and migration in a concentration-dependent manner (15.63–125 ppm). The hair growth index and growth area of the NS group (2.81 score, 81%) on day 14 were higher than those of the PC group (2.65 score, 68%) ( p < 0.05 ). Additionally, the HFs of the NS group were located deep in the subcutis, similar to the PC group with developed hair roots. Moreover, the mRNA expression of VEGF and IGF-1 was higher in the NS group compared to the PC group, whereas TGF-β1 expression was lower ( p < 0.05 ). Our findings indicate that NS modulates hair growth by increasing IGF-1 and VEGF expression while inhibiting that of TGF-β1. Therefore, our findings suggest that NS extract is a promising new hair loss treatment derived from a natural substance that helps promote hair growth and prevent hair loss.

scholarly journals The Expression and Significance of mTORC1 in Diabetic Retinopathy

2019 ◽  
Author(s):  
Yanli Liu ◽  
Yarong Zheng ◽  
Yekai Zhou ◽  
Yi Liu ◽  
Mengjuan Xie ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Diabetic Retinopathy ◽  
Western Blotting ◽  
Rat Model ◽  
High Glucose ◽  
Control Group ◽  
Diabetes Group ◽  
And Migration ◽  
Proliferation And Migration

Abstract Background: To investigate the expression and significance of mechanistic target of rapamycin complex 1(mTORC1) in diabetic retinopathy(DR), and to find new targets and new methods for the treatment of DR.Methods: A DR rat model was prepared by general feeding combined with intraperitoneal injection of 10% streptozotocin (60 mg/kg). The rats were randomly divided into a control group (NDM group) and diabetes group (DM group).Three months later,the degrees of retinopathy were determined using hematoxylin and eosin staining,and the levels of p-S6, VEGF, and PEDF proteins were detected by immunohistochemistry and western blotting. Human retinal capillary endothelial cells (HRCECs) were cultured in high glucose conditions,then treated with rapamycin or transfected with siTSC1.The protein levels of p-S6 were assessed by western blotting. The 5-ethynyl-2´-deoxyuridine assay was used to detect cell proliferation, and the Transwell assay was used to detect cell migration.Results: A DM rat model was successfully developed. The expressions of p-S6 and VEGF proteins were significantly increased in the DM group (p < 0.05), and the expression of PEDF protein was significantly decreased compared with the control group (p < 0.05). In vitro,the p-S6 protein in high glucose(HG) induced HRCECs was increased compared with the normal control (p < 0.05), and cell proliferation and migration were increased compared with the normal glucose(NG) group (p < 0.05). After transfection with siTSC1 to activate mTORC1,the expression of p-S6 was increased,as well as cell proliferation and migration.In contrast rapamycin decreased p-S6 expression in HG induced HRCECs, as well as decrased proliferation and migration (p < 0.05).Conclusion: The mTORC1 played an important role in DR. After activation, mTORC1 induced expression of the p-S6 protein, regulated the expressions of VEGF and PEDF proteins, and changed the proliferation and migration of endothelial cells.The mTORC1 can therefore be used as a new target,as well as in the treatment of DR.

scholarly journals Knockdown of Fibromodulin Inhibits Proliferation and Migration of RPE Cell via the VEGFR2-AKT Pathway

2018 ◽  
Vol 2018 ◽  
pp. 1-8 ◽  
Author(s):  
He Hu ◽  
Shanshan Li ◽  
Jianqiao Li ◽  
Chao Huang ◽  
Fang Zhou ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Retinal Pigment ◽  
Cell Counting ◽  
Control Group ◽  
Vegf Receptor ◽  
Phosphorylated Akt ◽  
And Migration ◽  
Proliferation And Migration

Purpose. Recent research has provided novel insight into the function of fibromodulin (FMOD) in wound healing and angiogenesis. The role of FMOD in initiation of proliferative vitreoretinopathy (PVR) has not been studied. This study investigated the effect of FMOD on human retinal pigment epithelial (RPE) cell, which plays an essential role in the progression of PVR, and the possible mechanisms. Methods. Small interfering (si) RNA-based gene transfer technology was used to decrease FMOD expression and to study its effects on RPEs in vitro. Cell Counting Kit-8 assays, transwells, and flow cytometry analysis were used to measure cell proliferation, migration, cell cycle, and apoptosis. Western blot was used to measure expression of vascular endothelial growth factor (VEGF), VEGF receptor 2 (VEGFR2), extracellular signal-related kinase 1/2 (ERK1/2), and phosphoinositide 3 kinase (PI3K/AKT). Results. After transfection of RPEs with a FMOD-specific siRNA, cell proliferation and migration were inhibited to the percentage of 65% ± 5% and 39% ± 10%, respectively, compared to the control group. Depletion of FMOD induced cell cycle arrest and apoptosis in RPE cells. Downregulation of VEGF, VEGFR2, and phosphorylated AKT (p-AKT) were detected in transfected RPEs. Conclusion. Depletion of FMOD selectively downregulated the expression of VEGF and VEGFR2 and inhibited the signaling pathway of AKT phosphorylation, which consequently inhibited the proliferation and migration of RPE Cell.

scholarly journals Autophagy-Sirtuin1(SIRT1) Modulated The Endothelial Progenitor Cells (EPCs) Proliferation and Migration Via wnt/β-Catenin/GSK3β Signaling Pathway and Alleviated The Coronary Atherosclerosis (CAS) in Mice

2021 ◽  
Author(s):  
Yanwei Li ◽  
Wei Cui ◽  
Bing Song ◽  
Xuying Ye ◽  
Zhuqing Li ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Cell Proliferation ◽  
Coronary Artery ◽  
Signaling Pathway ◽  
Pathological Condition ◽  
Control Group ◽  
And Migration ◽  
Sirt1 Activator ◽  
Proliferation And Migration

Abstract Background and purpose: SIRT1 exerted its link to CAS risk in humans and EPCs presented its reparative role in CAS. In this study, we explored the role of SIRT1 in CAS mice and also its modulation in EPCs.Methods and materials: ApoE-/- mice were fed with high-fat and high-glucose food to establish the CAS animal model with the normally-raised C57BL/6 mice as a healthy control group. 5 ApoE mice were intravenously injected with SIRT1 activator, SRT 2104 and another 5 were injected with inhibitor Nicotinamide in tail. Weight changes were recorded per week. Blood samples were taken from posterior orbital venous plexus and detected by automatic biochemical analyzer for lipid concentrations. Coronary artery tissues were observed. HE staining displayed the pathological condition while Immunohistochemistry (IHC) evaluated the CD34+/VEGFR2+ relative density. In vitro, EPCs were isolated from bone marrow each group and then purified, cultured and verified using immunofluorescence staining (IFS). Thereafter, we examined the modulatory mechanism of SIRT1 in EPCs by RT-PCR, MTT, Western Blot (WB) and colony formation, scratch methods, connecting the wnt/β-catenin/GSK3β signaling pathway.Results：SIRT1 activation negatively regulated the weight and TC, TG and LDL. SIRT1 activator alleviated the lesion area and decreased the CD34+/VEGFR2+ density which was higher in coronary artery tissues in CAS and SIRT1 inhibitor groups. In vitro, SIRT1 activator promoted the bone marrow-derived EPCs proliferation, migration and activated wnt/β-catenin/GSK3β signaling pathway while inhibited the autophagy biomarkers ATG1 and LC3II. Furthermore, inhibition of autophagy led to the upregulation of SIRT1 and increase in cell proliferation, migration and wnt/β-catenin/GSK3β activity. The suppression of the pathway in turn lowered SIRT1 expression in EPCs, attenuated the cell proliferation and migration and promoted autophagy. Conclusion: Taken all the findings together, this research disclosed that SIRT1 activator might perform its protective role in CAS through autophagy inhibition via wnt/β-catenin/GSK3β signaling pathway in EPCs.

scholarly journals Effects of Abnormal Savda Munzip on the Proliferation Activity and Migration Ability of Fibroblasts Derived from Hypertrophic Scar In Vitro

2015 ◽  
Vol 2015 ◽  
pp. 1-6 ◽  
Author(s):  
Hujun Wang ◽  
Weicheng Gao ◽  
Menglong Kong ◽  
Nan Li ◽  
Ma Shaolin
Keyword(s):  
Cell Structure ◽  
Fibroblast Cell ◽  
Control Group ◽  
Blank Control Group ◽  
Migration Ability ◽  
Migration Assay ◽  
Proliferation Activity ◽  
And Migration ◽  
Proliferation And Migration

Background. To explore the effect of ASMq on proliferation and migration ability of the fibroblast derived from HS of donor (HSFbs) in vitro.Methods. The HSFbs were cultured from tissue specimens and passaged to the 3~4 generation, which were treated with the different concentrations of ASMq and 5-Fu from 1 to 11 days. The difference of HSFbs proliferation activity was analyzed by the CCK-8 method. The HSFbs migration ability in ASMq (0.4 mg/mL) was analyzed by the Cell Scratch method.Results. Transmission electron microscope result shows ASMq concentration significantly increases and fibroblast cell structure markedly change in the experimental group. The proliferation activity of the HSFbs was obviously weakened in ASMq groups than those of the group A (P<0.05) at seven days. The group C (0.4 mg/mL) is better suitable than other three ASMq treatment groups. Cell Migration Assay shows that the migration ability HSFbs was significantly reduced in ASMq (0.4 mg/mL) treatment group compared with those of blank control group at both 24 h and 48 h (P<0.05).Conclusions. These results suggest that ASMq effectively restrains the proliferation and migration ability of the HTSFbs in vitro, which can be one of the mechanisms for the prevention and treatment of HS.

Chitinase-like protein YKL-40 regulates human bronchial epithelial cells proliferation, apoptosis, and migration through TGF-β1/Smads pathway

2019 ◽  
Vol 39 (4) ◽  
pp. 451-463 ◽  
Author(s):  
R Guan ◽  
R Lin ◽  
R Jin ◽  
L Lu ◽  
X Liu ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Apoptosis ◽  
Biological Behavior ◽  
Control Group ◽  
Bronchial Epithelial ◽  
Cell Proliferation And Migration ◽  
And Migration ◽  
Tgf Β1 ◽  
Cells Cultured ◽  
Proliferation And Migration

In order to study the effects of chitinase-like protein YKL-40 on proliferation, apoptosis, and migration of human bronchial epithelial cell line (BEAS-2B), and the underlying mechanisms, we cultured BEAS-2B alone or with different concentrations of YKL-40. thiazolyl blue tetrazolium bromide (MTT) assay was used to examine the cell proliferation. Annexin V-fluorescein isothiocyanate isomer (FITC)/propidium iodide staining and scratch assay were performed to test the cell apoptosis and migration. The concentrations of transforming growth factor-β1 (TGF-β1), Smad3, Smad7, alpha-smooth muscle actin (α-SMA), interleukin-4 (IL-4), IL-6, and IL-8 in the cell culture supernatant were detected by enzyme-linked immunosorbent assay. The messenger RNA and protein levels of YKL-40, TGF-β1, Smad3, Smad7, and α-SMA were detected by reverse transcription polymerase chain reaction and Western blot. BEAS-2B cells cultured with different concentrations of YKL-40 showed significantly higher cell proliferation and migration and inflammatory cytokines compared with that of control group, while the cell apoptosis was significantly lower than that of control group ( p < 0.05). In addition, BEAS-2B cells cultured with YKL-40 had increased TGF-β1, Smad3, Smad7, and α-SMA levels in the supernatant, compared with that of BEAS-2B cells cultured alone ( p < 0.05). Furthermore, LY364947, as TGF-β1/Smads signaling pathway inhibitor, decreased cell proliferation and migration ability and enhanced cell apoptosis of BEAS-2B cells compared with control group ( p < 0.05). However, YKL-40 administration reversed the effect of LY364947 on the biological behavior of BEAS-2B cells. YKL-40 could affect the biological behaviors of BEAS-2B cells, which might be related to the TGF-β1/Smads pathway.

scholarly journals CSTB Downregulation Promotes Cell Proliferation and Migration and Suppresses Apoptosis in Gastric Cancer SGC-7901 Cell Line

2016 ◽  
Vol 24 (6) ◽  
pp. 487-494 ◽  
Author(s):  
Jian Zhang ◽  
ZhenFeng Shi ◽  
JinXing Huang ◽  
XiaoGuang Zou
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Control Group ◽  
Human Gastric Cancer ◽  
Cell Proliferation And Migration ◽  
And Migration ◽  
Development Of Gastric Cancer ◽  
Proliferation And Migration

This study aimed to investigate the pivotal role of cystatin B (CSTB) in the development of gastric cancer and to explore its possible regulatory mechanism. Human gastric cancer SGC-7901 cells as a model in vitro were transfected with plasmid PCDNA3.1-CSTB and siRNA-CSTB using Lipofectamine 2000. Quantitative real-time PCR (qRT-PCR) and Western blotting were performed to determine the relative expression of CSTB and PI3K/Akt/mTOR pathway-related protein. Moreover, MTT assay, Transwell assay, and flow cytometry were used to assess cell proliferation, migration, and apoptosis, respectively. The results showed that CSTB was significantly downregulated in SGC-7901 cells compared with gastric epithelial cells. CSTB was successfully overexpressed and suppressed after cells were transfected with pc-CSTB and si-CSTB, respectively. Moreover, cell viability and migration were significantly decreased after being transfected with pc-CSTB when compared with the control group, while being obviously increased after transfection with si-CSTB. However, cell apoptosis was significantly induced after being transfected with pc-CSTB, while being obviously suppressed after transfection with si-CSTB. Besides, the expression levels of p-PI3K, p-Akt, and p-mTOR proteins were all significantly decreased in the pc-CSTB transfection group when compared with the control group, while being increased in the si-CSTB transfection group. Our findings suggest that CSTB downregulation may promote the development of gastric cancer by affecting cell proliferation and migration, and the PI3K/Akt/mTOR signaling pathway was activated in this process. CSTB may serve as a potential therapeutic target for gastric cancer.

Platelet-Derived Exosomes Affect the Proliferation and Migration of Human Umbilical Vein Endothelial Cells Via miR-126

2019 ◽  
Vol 17 (4) ◽  
pp. 379-387 ◽  
Author(s):  
Yan Sun ◽  
Xiao-li Liu ◽  
Dai Zhang ◽  
Fang Liu ◽  
Yu-jing Cheng ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Growth Factor ◽  
Real Time ◽  
Umbilical Vein ◽  
Angiogenic Factors ◽  
Healthy Donors ◽  
And Migration ◽  
Umbilical Vein Endothelial Cells ◽  
Tgf Β1 ◽  
Proliferation And Migration

Background:Intraplaque angiogenesis, the process of generating new blood vessels mediated by endothelial cells, contributes to plaque growth, intraplaque hemorrhage, and thromboembolic events. Platelet-derived Exosomes (PLT-EXOs) affect angiogenesis in multiple ways. The ability of miR-126, one of the best-characterized miRNAs that regulates angiogenesis, carried by PLT-EXOs to influence angiogenesis via the regulation of the proliferation and migration of endothelial cells is unknown. In this study, we aimed to investigate the effects of PLT-EXOs on angiogenesis by Human Umbilical Vein Endothelial Cells (HUVECs).Methods:We evaluated the levels of miR-126 and angiogenic factors in PLT-EXOs from Acute Coronary Syndrome (ACS) patients and healthy donors by real-time Polymerase Chain Reaction (PCR) and western blotting. We incubated HUVECs with PLT-EXOs and measured cell proliferation and migration with the Cell Counting Kit-8 assay and scratch assay, respectively. We also investigated the expression of miR-126 and angiogenic factors in HUVECs after exposure to PLT-EXOs by western blotting and real-time PCR.Results:PLT-EXOs from ACS patients contained higher levels of miR-126 and angiogenic factors, including Vascular Endothelial Growth Factor (VEGF), basic Fibroblast Growth Factor (bFGF), and Transforming Growth Factor Beta 1 (TGF-β1), than those from healthy donors (p<0.05). Moreover, the levels of exosomal miR-126 and angiogenic factors were increased after stimulation with thrombin (p<0.01). HUVEC proliferation and migration were promoted by treatment with activated PLT-EXOs (p<0.01); they were accompanied by the over-expression of miR-126 and angiogenic factors, including VEGF, bFGF, and TGF-β1 (p<0.01).Conclusion:Activated PLT-EXOs promoted the proliferation and migration of HUVECs, and the overexpression of miR-126 and angiogenic factors, thereby elucidating potential new therapeutic targets for intraplaque angiogenesis.

Investigation of Oral Subacute Toxicity and In-Vitro Antioxidant Activity of Standardized Methanolic Extract of Quercus serrata Leaves

2020 ◽  
Vol 16 ◽  
Author(s):  
Maibam Beebina Chanu ◽  
Biseshwori Thongam ◽  
Khumukcham Nongalleima ◽  
Hans Raj Bhat ◽  
Surajit Kumar Ghosh ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Antioxidant Activity ◽  
Biochemical Parameters ◽  
Methanolic Extract ◽  
Reducing Power ◽  
Quercus Serrata ◽  
Control Group ◽  
Blood Cell Count ◽  
Toxicological Profile

Background: Quercus serrata Murray leaves have been used traditionally in the treatment of diabetes, dysmenorrhoea, inflammation and urinary tract infection. So, far no study had been reported on the toxicological profile and antioxidant properties of the plant. Objective: The present study was aimed to investigate the in-vivo toxicological profile and in-vitro antioxidant activities of the methanolic extract of standardized Quercus serrata leaves. Methods: Per-oral sub-acute toxicity study was performed in rats using three dose levels (200, 400 and 800 mg/kg b.w.) of the extract for 28-days. Control group received gum acacia suspended in water. Bodyweight was measured weekly. Biochemical parameters were analysed using the serum, the blood-cell count was done using whole blood. Pathological changes were also checked in highly perfused tissues. Further, in-vitro reducing power assay, nitric oxide scavenging assay, DPPH free-radical scavenging assay were performed to check the antioxidant activity of the extract. Results: There were no significant alterations in the blood-cell count and biochemical parameters analysed in the treatment group when compared with the normal control. Histopathology study of liver, kidney, pancreas, heart and brain revealed normal cellular architecture in the treatment groups alike the control group animals. Quercus serrata also showed a significant reduction of DPPH with IC50 4.48±0.254 µg/mL, in-vitro reducing power activity with IC50121.65±0.320 µg/mL and nitric oxide scavenging activity IC50 106.43±0.338 µg/mL. Conclusion: The above study showed that standardized methanolic extract of Quercus serrata leaves was safe after subacute oral administration in rats and has good antioxidant potential.

scholarly journals Hypoxic glioma-derived exosomes promote M2-like macrophage polarization by enhancing autophagy induction

2021 ◽  
Vol 12 (4) ◽  
Author(s):  
Jianye Xu ◽  
Jian Zhang ◽  
Zongpu Zhang ◽  
Zijie Gao ◽  
Yanhua Qi ◽  
...  
Keyword(s):  
Macrophage Polarization ◽  
Autophagy Induction ◽  
Antitumor Immunotherapy ◽  
Novel Biomarkers ◽  
And Migration ◽  
Immunosuppressive Microenvironment ◽  
Proliferation And Migration ◽  
Glioma Progression

AbstractExosomes participate in intercellular communication and glioma microenvironment modulation, but the exact mechanisms by which glioma-derived exosomes (GDEs) promote the generation of the immunosuppressive microenvironment are still unclear. Here, we investigated the effects of GDEs on autophagy, the polarization of tumor-associated macrophages (TAMs), and glioma progression. Compared with normoxic glioma-derived exosomes (N-GDEs), hypoxic glioma-derived exosomes (H-GDEs) markedly facilitated autophagy and M2-like macrophage polarization, which subsequently promoted glioma proliferation and migration in vitro and in vivo. Western blot and qRT-PCR analyses indicated that interleukin 6 (IL-6) and miR-155-3p were highly expressed in H-GDEs. Further experiments showed that IL-6 and miR-155-3p induced M2-like macrophage polarization via the IL-6-pSTAT3-miR-155-3p-autophagy-pSTAT3 positive feedback loop, which promotes glioma progression. Our study clarifies a mechanism by which hypoxia and glioma influence autophagy and M2-like macrophage polarization via exosomes, which could advance the formation of the immunosuppressive microenvironment. Our findings suggest that IL-6 and miR-155-3p may be novel biomarkers for diagnosing glioma and that treatments targeting autophagy and the STAT3 pathway may contribute to antitumor immunotherapy.

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