Yun, Jong-Kuk;Yoon, Hye-Eun;Park, Jeong-Kyu;Kim, Mi Ryeo;Kim, Dae-Ik
Journal of the Society of Cosmetic Scientists of Korea
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v.41
no.4
/
pp.401-411
/
2015
This study was performed to investigate the wound healing effect of skin regeneration cosmetics utilizing low molecular weight Polydeoxynucleotide (PDRN). High purity PDRN was prepared from salmon testes poly-deoxy-ribonucleotide through protein and toxin removal process and molecular weight reduction. In order to evaluate the wound healing effect of PDRN in SD rats, 4 sites of dorsal skin of each animal were excised by using biopsy punch and $500{\mu}L$ of test solution was topically applied once daily for 4 weeks. The tissue changes were observed for every week during the application periods. After applying the PDRN to the wound, the skin was cut flower and contraction of the wounds more quickly, and the coating of PDRN in the wound area was reduced significantly as compared to the positive control group $Fucidin^{(R)}$ applied. The microscopic observation of stained tissue showed that a positive control was most rapid in re-epithelialization ability followed by the PH group, PDRN group, HA group. In addition, transforming growth factor ($TGF-{\beta}$) and vascular endothelial growth factor (VEGF), such as in the growth factor was similar to the results of staining of tissue lesions. In conclusion, it is determined that the low molecular weight PDRN has the therapeutic effect to the wound, and could be used as a functional material of cosmetics and medical industries.
Ha, Soo-Min;Kim, Jung-Sook;Kim, Ji-Hyeon;Kim, Do-Yeon
Journal of the Korean Applied Science and Technology
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v.35
no.4
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pp.1096-1107
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2018
The purpose of this study was to investigate the effects of combined exercise on blood inflammatory factors, DHEA-s and arterial stiffness in elderly women. The subjects were 42 elderly females volunteers, aged 70 to 85 years, composed of the combined exercise group (n=21) and control group (n=21). The 60 minute combined exercise program(aquarobics 1 time/week, strength exercise 2 times/week) was performed 3 times per week for 12 weeks, and the intensity was progressively increased every 4 weeks(1-4 weeks: RPE 12 to 13, 5-8 weeks: RPE 13 to 14, 9-12weeks: RPE 14 to 15). The test data were analyzed by two-way repeated measures ANOVA, paired t-test, independent t-test and the alpha level of .05 was set for all tests of significance. As a result, the combined exercise for 12 weeks reduced the inflammatory response of elderly women, and DHEA-s was found to have a positive effect on aging hormone. The arterial stiffness decreased the central arterial blood pressure (systolic and diastolic), prevented the increase of the pulse pressure and the wave increase index, and decreased the pulse wave velocity. These results suggest that regular and continuous combined exercise may be recommended for the healthy aging and longevity of elderly women by inducing anti-inflammation effect and improving the aging hormonal function and the vascular health.
Arterial thrombosis and its associated diseases are considered to constitute a major healthcare problem. Arterial thrombosis, defined as blood clot formation in an artery that interrupts blood circulation, is associated with many cardiovascular diseases. Oxidative stress is one of many important factors that aggravates the pathophysiological process of arterial thrombosis. Apurinic/apyrimidinic endonuclease 1/redox factor-1 (Ref-1) has a multifunctional role in cells that includes the regulation of oxidative stress and anti-inflammatory function. The aim of this study was to investigate the therapeutic effect of adenovirus-mediated Ref-1 overexpression on arterial thrombosis induced by 60% FeCl3 solution in rats. Blood flow was measured to detect the time to occlusion, thrombus formation was detected by hematoxylin and eosin staining, reactive oxygen species (ROS) levels were detected by high-performance liquid chromatography, and the expression of tissue factor and other proteins was detected by Western blot. FeCl3 aggravated thrombus formation in carotid arteries and reduced the time to artery occlusion. Ref-1 significantly delayed arterial obstruction via the inhibition of thrombus formation, especially by downregulating tissue factor expression through the Akt-GSK3β-NF-κB signaling pathway. Ref1 also reduced the expression of vascular inflammation markers ICAM-1 and VCAM-1, and reduced the level of ROS that contributed to thrombus formation. The results showed that adenovirus-mediated Ref-1 overexpression reduced thrombus formation in the rat carotid artery. In summary, Ref-1 overexpression had anti-thrombotic effects in a carotid artery thrombosis model and could be a target for the treatment of arterial thrombosis.
Kim, Tae-Hoon;Kim, Ji-Yoon;Bae, Jieun;Kim, Young-Mi;Won, Moo-Ho;Ha, Kwon-Soo;Kwon, Young-Guen;Kim, Young-Myeong
Journal of Ginseng Research
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v.45
no.2
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pp.344-353
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2021
Background: Korean Red ginseng extract (KRGE) has beneficial effects on the cardiovascular system by improving endothelial cell function. However, its pharmacological effect on endothelial cell senescence has not been clearly elucidated. Therefore, we examined the effect and molecular mechanism of KRGE on the senescence of human umbilical vein endothelial cells (HUVECs). Methods: HUVECs were grown in normal or KRGE-supplemented medium. Furthermore, they were transfected with heme oxygenase-1 (HO-1) gene or treated with its inhibitor, a NF-κB inhibitor, and a miR-155-5p mimic or inhibitor. Senescence-associated characteristics of endothelial cells were determined by biochemical and immunohistochemical analyses. Results: Treatment of HUVECs with KRGE resulted in delayed onset and progression of senescence-associated characteristics, such as increased lysosomal acidic β-galactosidase and decreased telomerase activity, angiogenic dysfunction, and abnormal cell morphology. KRGE preserved the levels of anti-senescent factors, such as eNOS-derived NO, MnSOD, and cyclins D and A: however, it decreased the levels of senescence-promoting factors, such as ROS, activated NF-κB, endothelial cell inflammation, and p21 expression. The beneficial effects of KRGE were due to the induction of HO-1 and the inhibition of NF-κB-dependent biogenesis of miR-155-5p that led to the downregulation of eNOS. Moreover, treatment with inhibitors of HO-1, NF-κB, and miR-155-5p abolished the anti-senescence effects of KRGE. Conclusion: KRGE delayed or prevented HUVEC senescence through a signaling cascade involving the induction of HO-1, the inhibition of NF-κB-dependent miR-155-5p biogenesis, and the maintenance of the eNOS/NO axis activity, suggesting that it may protect against vascular diseases associated with endothelial senescence.
Park, Hye Rim;Kim, Ha Yeon;Kim, Jin Young;Oh, Sinseok;Kang, Pilsun;Lee, Gang Hyuk;Lim, Jung-Hyurk;Shin, Song Seok
Journal of the Society of Cosmetic Scientists of Korea
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v.48
no.2
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pp.169-180
/
2022
Streptococcus sp. is generally known as a strain that produces hyaluronic acid. In this study, we focused on ingredients other than hyaluronic acid among several metabolites produced by Streptococcus sp. during cultivation. The hair experimental sample (HAIRCLETM) was prepared with Streptococcus sp. culture filtrate under the condition that hyaluronic acid was not produced and the effect on the hair was identified. Tensile strength of hair was tested with a universal testing machine (UTM). Surface properties of a hair were examined with an atomic force microscope (AFM). Our results suggest that HAIRCLETM could prevent damage to a hair such as destroyed-cuticle, increased-faction force, and broken-hair. Furthermore, hair-related experiments confirmed that HAIRCLETM could promote the expression of hair growth factors VEGF, HGF, and Wnt10b and mitigate male hair loss by inhibiting androgen receptors and TGF-β2 expression. In addition, it was confirmed that the expression of barrier-related factors (INV, CLDN-1) was increased for oxidative stress, and the COX-2 expression, an inflammatory factor, was inhibited, thereby improving damaged scalp barriers and alleviating induced inflammation.
Hwang, In Seung;Kim, Young Jin;Park, Yun Soo;Kim, Hyun Ju;Kim, Do Hoon;Park, Wan Su
The Korea Journal of Herbology
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v.29
no.4
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pp.83-89
/
2014
Objectives : The purpose of this study was to investigate effects of Houttuyniae Herba water extract (HC) on calcium release and production of various inflammatory mediators such as nitric oxide (NO), interferon-inducible protein (IP)-10, platelet derived growth factor (PDGF)-BB, keratinocyte-derived chemokine (KC), vascular endothelial growth factor (VEGF), interleukin (IL)-4, and IL-5 in lipopolysaccharide (LPS)-induced RAW 264.7 mouse macrophages. Methods : NO production was measured by Griess reagent assay. Intracellular calcium level was measured with Fluo-4 assay. Levels of cytokines were measured by High-throughput multiplex bead array cytokine assay based on xMAP (multi-analyte profiling beads) technology. Results : HC significantly decreased NO production for 24 hrs incubation at the concentrations of 10, 25, 50, 100, and $200{\mu}/mL$ in LPS-induced RAW 264.7 (P < 0.05). HC significantly decreased production of IP-10, KC, VEGF, and PDGF-BB for 24 hrs incubation at the concentrations of 50, 100, and $200{\mu}/mL$ in LPS-induced RAW 264.7 (P < 0.05). HC also significantly decreased intracellular calcium release for 24 hrs incubation at the concentrations of 25, 50, 100, and $200{\mu}/mL$ in LPS-induced RAW 264.7 (P < 0.05). But HC did not show any significant effect on production of IL-4 and IL-5 in LPS-induced RAW 264.7. Conclusions : The results suggested that HC has anti-inflammatory property related with its inhibition on the production of NO, IP-10, KC, VEGF, and PDGF-BB in LPS-induced macrophages via calcium pathway.
Objective : Patients with mild ischemic stroke experience various sequela and residual symptoms, such as anxious behavior and deficits in movement. Few approaches have been proved to be effective and safe therapeutic approaches for patients with mild ischemic stroke by acute stroke. Sildenafil (SIL), a phosphodiesterase-5 inhibitor (PDE5i), is a known remedy for neurodegenerative disorders and vascular dementia through its angiogenesis and neurogenesis effects. In this study, we investigated the efficacy of PDE5i in the emotional and behavioral abnormalities in rats with mild ischemic stroke. Methods : We divided the rats into four groups as follows (n=20, respectively) : group 1, naïve; group 2, middle cerebral artery occlusion (MCAo30); group 3, MCAo30+SIL-pre; and group 4, MCAo30+SIL-post. In the case of drug administration groups, single dose of PDE5i (sildenafil citrate, 20 mg/kg) was given at 30-minute before and after reperfusion of MCAo in rats. After surgery, we investigated and confirmed the therapeutic effect of sildenafil on histology, immunofluorescence, behavioral assays and neural oscillations. Results : Sildenafil alleviated a neuronal loss and reduced the infarction volume. And results of behavior task and immunofluorescence shown possibility that anti-inflammation process and improve motor deficits sildenafil treatment after mild ischemic stroke. Furthermore, sildenafil treatment attenuated the alteration of theta-frequency rhythm in the CA1 region of the hippocampus, a known neural oscillatory marker for anxiety disorder in rodents, induced by mild ischemic stroke. Conclusion : PDE5i as effective therapeutic agents for anxiety and movement disorders and provide robust preclinical evidence to support the development and use of PDE5i for the treatment of mild ischemic stroke residual disorders.
The expression of interleukin-1α (IL-1α) is elevated in monocytic cells, such as monocytes and macro-phages, within atherosclerotic arteries, yet the cellular molecules involved in cytokine upregulation remain unclear. Because peptidoglycan (PG), a major component of gram-positive bacterial cell walls, is detected within the inflammatory cell-rich regions of atheromatous plaques, it was investigated if PG contributes to IL-1α expression in monocytes/macrophages. Exposure of THP-1 monocytic cells to PG resulted in elevated levels of IL-1α gene transcripts and increased secretion of IL-1α protein. The transcription and secretion of IL-1α were abrogated by OxPAPC, an inhibitor of TLR2/4, but not by polymyxin B that inhibits lipopolysaccharide-induced TLR4 activation. To understand the molecular mechanisms of the inflammatory responses due to bacterial pathogen-associated molecular patterns (PAMPs) in diseased arteries, we attempted to determine the cellular factors involved in the PG-induced upregulation of IL-1α expression. Pharmacological inhibition of cell signaling pathways with LY294002 (a PI3K inhibitor), Akti IV (an inhibitor of Akt activation), rapamycin (an mTOR inhibitor), U0126 (a MEK inhibitor), SB202190 (a p38 MAPK inhibitor), SP6001250 (a JNK inhibitor), and DPI (a NOX inhibitor) also significantly attenuated the PG-mediated expression of IL-1α. These results suggest that PG induces the monocytic or macrophagic expression of IL-1α, thereby contributing to vascular inflammation, via multiple signaling molecules, including TLR2, PI3K/Akt/mTOR, and MAPKs.
Objectives: This study aimed to examine the safety, effects on proliferation of hair papilla cells, and anti-inflammatory and antioxidant mechanisms of Artemisia sieversiana Ehrh. ex Willd. (AS) extract. Methods: Safety tests through purity testing, acute toxicity tests, and repeated toxicity tests were performed using AS extract (ASE) which had been dried for over two years. Cell culture and proliferation tests were conducted; VEGF (vascular endothelial growth factor), bFGF (basic fibroblast growth factor), and EGF (epidermal growth factor) and protein expression analyses were performed for mechanistic evaluation; and inhibitory effects of ASE on the RNA expression of testosterone, 5𝛼-reductase, and aromatase was assessed. The anti-inflammatory and antioxidant efficacy of ASE was confirmed by measuring the levels of nitric oxide, inflammatory mediators (TNF-𝛼 and PGE2), inflammatory cytokines (IL-1𝛽, IL-6, and IL-8), and chemokine MCP-1. Results: The safety of ASE was confirmed. The mechanism of cell proliferation in human hair follicle dermal papilla cells involved the promotion of VEGF, bFGF, and EGF expression. ASE decreased mRNA expression of testosterone, 5𝛼-reductase, and aromatase-1 in a concentration-dependent manner. PGE2 and TNF-𝛼 production by inflammatory mediators was also significantly decreased in a concentration-dependent manner, and inflammatory cytokine and chemokine expression was inhibited. Conclusions: ASE is suggested to promote papillary cell growth at the cellular level, to suppress expression of various enzymes involved in hair cycle and cell death, and to inhibit hair loss through anti-androgen, anti-inflammatory, and antioxidant effects.
Long-chain fatty acids (LCFAs) are vital in cellular compartments, primarily regulating lipid metabolism. Fatty Acid-Binding Proteins (FABPs) facilitate LCFA transport, lipid synthesis, storage, and act as signaling molecules influencing various pathways, including inflammation. FABP4, in particular, is linked to vascular and cardio-related diseases, and it plays a role in macrophage-mediated inflammatory responses. Previous studies have identified FABP4 as not only a representative biomarker for lipogenesis but also as having correlations with immune responses. This study aims to investigate the regulation of the chicken FABP4 (chFABP4) gene by toll-like receptor 3 (TLR3) activation and determine the signaling pathways that are involved in chFABP4 transcriptional regulation. We analyzed the transcriptional regulation of chFABP4 in TLR3-stimulated DF-1 cells. The results showed that chFABP4 was up-regulated upon stimulation with polyinosinic-polycytidylic acid (PIC), a TLR3 ligand. Notably, chFABP4 transcription was independently regulated in the NF-κB signaling pathway. It was up-regulated in p38 inhibition, demonstrating that the p38 signaling pathway might suppress the transcription of chFABP4 within TLR3-activated DF-1 cells. In contrast, chFABP4 expression was down-regulated in JNK signaling pathway inhibition, suggesting the positive regulation of JNK signaling pathway for chFABP4 transcription in DF-1 cells in response to TLR3 activation, consistent with findings in macrophages. MEK pathway inhibition resulted in a similar regulation to NF-κB signaling. These results suggest that each MAPK contributes differentially to the transcriptional regulation of chFABP4 by in DF-1 cells in response to TLR3 activation.
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