• Current Research on Agriculture and Life Sciences
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• v.32 no.3
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• pp.119-124
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• 2014

Physalis alkekengi var. francheti Hort. is known as an insecticide and traditional remedy for liver related diseases. Therefore, this study investigated the chemopreventive effects of extracts and several solvent fractions (n-hexane, dichloromethane, n-butanol, water) of Physalis alkekengi var. francheti Hort. First, their cytotoxicity and NQO1 activity were measured using an MTT assay, plus a quinone reductase [NAD(P)H dehydrogenase (quinone); NAD(P)H: (quinone acceptor) oxidoreductase, EC 1.6.99.2]-inducing activity assay was performed using cultured murine hepatoma cells (Hepa1c1c7) and its mutant cells(BpRc1). The reduction of electrophilic quinones by NQO1 is an important detoxification pathway and major mechanism of chemoprevention. When compared with the other solvent soluble fractions with different polarities, the dichloromethane fraction of Physalis alkekengi var. francheti Hort. showed a higher NQO1-inducing activity that was also dose-dependent. Moreover, the dichloromethane fraction of Physalis alkekengi var. francheti Hort. induced ARE-luciferase activities in HepG2-C8 cells that were generated by transfecting the ARE-luciferase gene construct, suggesting the Nrf2-ARE-mediated induction of anti-oxidative enzymes. In conclusion, the dichloromethane-soluble fraction of Physalis alkekengi var. francheti Hort. showed a relatively strong induction of detoxifying enzymes, thereby meriting further study to identify the active components and evaluate their potential as cancer preventive agents.

• Journal of The Korean Dental Society of Anesthesiology
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• v.14 no.2
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• pp.107-114
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• 2014

Background: Angiogenesis has been recognized an essential precondition for osteogenesis. Because reduction and disruption of the blood supply to tissue cause tissue hypoxia, pathological bone loss affected by hypoxia often can occur in various clinical conditions. The effects of propofol on the process of osteogenesis have received little direct attention. Therefore, we investigated the effect of propofol on the growth and function of osteoblasts under hypoxic condition. Methods: After propofol (3, 30, $300{\mu}M$) preconditioning for 2 hours, hFOB 1.19 human osteoblast cells were cultured under 1 % oxygen tension for 48 hours. Using real time PCR and western blot analysis, we analyzed the expression of, BMP-2, TGF-${\beta}1$, type I collagen, osteocalcin, HIF-1s and Akt. Cell viability was also determined by MTT assay. Results: Propofol preconditioning on hypoxic-cultured osteoblast promoted the expressions of BMP-2, TGF-${\beta}1$, type I collagen and osteocalcin and induced hypoxia-mediated HIF-1 activation and the expression of Akt protein. Propofol with $300{\mu}M$ significant decreased cell viability compared to control. Conclusions: Clinically relevant concentrations of propofol are not cytotoxic to hypoxic osteoblasts in vitro. Propofol preconditioning on hypoxic-cultured osteoblast stimulates proliferation and differentiation of osteoblast through induced expression of BMP-2, TGF-${\beta}1$, type I collagen and osteocalcin. Propofol might promote angiogenesis and bone regeneration under hypoxic condition.

• Journal of Dental Anesthesia and Pain Medicine
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• v.19 no.5
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• pp.253-260
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• 2019

Background: Sometimes general anesthesia is required for dental surgery in pregnant women. Facial bone fractures or neck abscess should be treated immediately. Dental surgery, however, creates a stressful situation that can cause inflammation. Inflammatory responses are a well-known major cause of preterm labor and preterm birth. Here we demonstrate the effects of remifentanil on the factors related to preterm labor and its mechanism of action on amniotic-derived epithelial cells (WISH cells). Methods: WISH cells were exposed to lipopolysaccharide (LPS) for 24 h and co-treated with various concentrations of remifentanil. MTT assays were performed to measure cell viability. To explain the effects of remifentanil on the factors related to inflammation in WISH cells, activation of nuclear factor kappa B ($NF-{\kappa}B$) and p38 and the expression of interleukin $(IL)-1{\beta}$, tumor necrosis factor $(TNF)-{\alpha}$, cyclooxygenase (COX)2, and prostaglandin E $(PGE)_2$ were quantified using western blotting and RT-PCR, respectively. Results: Remifentanil did not affect WISH cell viability. In western blot analysis, co-treatment with remifentanil resulted in decreased phosphorylation of $NF-{\kappa}B$, and expression of COX2 and $PGE_2$ in LPS-induced inflammation, but the results were statistically significant only at low concentrations. Reduction of $IL-1{\beta}$ and $TNF-{\alpha}$ expression was also observed with RT-PCR. Conclusion: Co-treatment with remifentanil does not affect the viability of WISH cells, but reduces the expression of the factors related to inflammation, which can induce uterine contraction and preterm labor. These findings provide evidence that remifentanil may inhibit uterine contraction and preterm labor in clinical settings.

• Journal of dental hygiene science
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• v.19 no.2
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• pp.141-146
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• 2019

Background: Oral cancer has a high incidence worldwide and has been closely associated with smoking, alcohol, and infection by the human papillomavirus. Metastasis is highly important for oral cancer survival. Lysophosphatidic acid (LPA) is a bioactive lipid mediator that promotes various cellular processes, including cell survival, proliferation, metastasis, and invasion. Signal transducer and activator of transcription (STATs) are transcription factors that mediate gene expression. Among the seven types of STATs in mammals, STAT3 is involved in invasion and metastasis of numerous tumors. However, little is known about the role of STAT3 in oral tumor invasion. In the present study, we hypothesized that STAT3 mediates LPA-induced oral cancer invasion. Methods: Immunoblotting was performed to analyze LPA-induced STAT3 activation. 3-(4,5-Dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) assay was performed to assess the survival rates of YD-10B cells. STAT3 levels in LPA-treated oral tumor cells were evaluated by performing in vitro invasion assay. Results: To the best of our knowledge, this is the first study to demonstrate that LPA enhances STAT3 phosphorylation in oral cancer. In addition, treatment with WP1066, a selective inhibitor of STAT3, at a concentration that does not cause severe reduction in cell viability, significantly attenuated LPA-induced YD-10B cancer cell invasion. Conclusion: The results suggested that LPA induces oral tumor cells with greater invasive potential via STAT3 activation. Our findings provided important insights into the mechanisms underlying mouth neoplasms.

• Journal of the Korean Applied Science and Technology
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• v.37 no.6
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• pp.1545-1555
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• 2020

In the present study, we investigated the antioxidant activity of Aucklandia lappa Decne (AL). Cell viability was measured in an MTT assay. Antioxidant effects were evaluated based on total polyphenol/flavonoid contents, ABTS radical scavenging activity, DPPH radical scavenging activity, SOD activity, and ROS content. AL was found not to be toxic at concentrations of 1 ㎍/mL, 10 ㎍/mL, and 100 ㎍/mL, respectively. The phenolic content was higher in AL-D than in AL-E, while the flavonoid content was higher in AL-E than in AL-D. AL-E exhibited higher ABTS radical scavenging activity than AL-D, and the EC50 values for BHA were 217.1 ㎍/mL in AL-D and 180.5 ㎍/mL in AL-E. AL-E also showed the highest DPPH radical scavenging activity. EC50 values for BHA were 114.2 ㎍/mL in AL-D and 95.8 ㎍/mL in AL-E. The SOD-like activity of AL-E was higher than that of AL-D. The EC50 values for ascorbic acid were 48.5 ㎍/mL in AL-D and 72.9 ㎍/mL in AL-E, indicating that both AL extracts have a SOD activity higher than that of ascorbic acid. AL-E reduced relatively more ROS than AL-D. With 100 ㎍/mL AL-E, the reduction level was almost similar to that of dexamethasone. Our results demonstrate that AL have antioxidant effects, and we believe that they could be very valuable as raw materials for anti-aging products, based on their antioxidant activity.

• The Korea Journal of Herbology
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• v.28 no.6
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• pp.79-86
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• 2013

Objectives : The purpose of this study is to investigate neuroprotective effects and molecular mechanisms of luteolin against ${\beta}$-amyloid ($A{\beta}_{25-35}$)-induced oxidative cell death in BV-2 cells. Methods : The protective effects of luteolin against $A{\beta}_{25-35}$-induced cytotoxicity and apoptotic cell death were determined by MTT dye reduction assay and TUNEL staining, respectively. The apoptotic cell death was further analyzed by measuring mitochondrial transmembrane potential and expression of pro- and/or anti-apoptotic proteins. To elucidate the molecular mechanisms underlying the protective effects of luteolin, intracellular accumulation of reactive oxygen species, oxidative damages, and expression of antioxidant enzymes were examined. Results : Luteolin pretreatment effectively attenuated $A{\beta}_{25-35}$-induced apoptotic cell death indices such as DNA fragmentation, dissipation of mitochondrial transmembrane potential, increased Bax/Bcl-2 ratio, and activation of c-Jun N-terminal kinase and caspase-3 in BV-2 cells. Furthermore, $A{\beta}_{25-35}$-induced intracellular formation of reactive oxygen species and subsequent oxidative damages such as lipid peroxidation and depletion of endogenous antioxidant glutathione were suppressed by luteolin treatment. The neuroprotective effects of luteolin might be mediated by up-regulation of cellular antioxidant defense system via up-regulation of ${\gamma}$-glutamylcysteine ligase, a rate-limiting enzyme in the glutathione biosynthesis and superoxide dismutase, an enzyme involved in dismutation of superoxide anion into oxygen and hydrogen peroxide. Conclusions : These findings suggest that luteolin has a potential to protect against $A{\beta}_{25-35}$-induced neuronal cell death and damages thereby exhibiting therapeutic utilization for the prevention and/or treatment of Alzheimer's disease.

• The Korea Journal of Herbology
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• v.34 no.6
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• pp.117-124
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• 2019

Objective : Broccoli is edible green plant that has a wide variety of health benefits including cancer prevention and cholesterol reduction. However, leaves of broccoli are not eaten and are mostly left as waste. This study was conducted to evaluate the effects of the broccoli leaf extract (BLE) on prostaglandin E₂ (PGE₂) production related to nuclear factor kappa B (NF-κB) signaling in lipopolysaccharide (LPS)-activated macrophages. Methods : BLE was prepared by extracting dried leaf with ethanol. Cell viability was determined by 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. PGE₂ and inflammatory cytokines were detected by enzyme-linked immunosorbent assay (ELISA). Expression level of each protein was monitored by Western blot analysis. Results : In LPS-activated Raw264.7 cells, PGE₂ release into culture medium was dramatically enhanced compared to control cells. However, increased PGE₂ was attenuated dose-dependently by treatment with BLE. Inhibition of PGE₂ production by BLE was due to the suppression of cyclooxygenase-2 (COX-2) expression determined by Western blot analysis. BLE also inhibited the production of inflammatory cytokines such as interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α). Inhibition at PGE₂ and cytokine was mediated from inhibition of nuclear translocation of NF-κB due to the repression of inhibitory kappa B alpha (IκBα) phosphorylation and degradation. Conclusion : This study showed that BLE exerted inhibitory activities against PGE₂, which is critical for the initiation and resolution of inflammatory responses, and that inhibition of PGE₂ was mediated by suppression of NF-κB signaling. These results suggest that the waste broccoli leaves could be used for controlling inflammation.

• Journal of Ginseng Research
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• v.47 no.3
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• pp.479-491
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• 2023

Background: Hepatocellular carcinoma (HCC) has a high incidence and is one of the highest mortality cancers when advanced stage is proceeded. However, Anti-cancer drugs available for treatment are limited and new anti-cancer drugs and new ways to treat them are minimal. We examined that the effects and possibility of Red Ginseng (RG, Panax ginseng Meyer) as new anti-cancer drug on HCC by combining network pharmacology and molecular biology. Materials and Methods: Network pharmacological analysis was employed to investigate the systems-level mechanism of RG focusing on HCC. Cytotoxicity of RG was determined by MTT analysis, which were also stained by annexin V/PI staining for apoptosis and acridine orange for autophagy. For the analyze mechanism of RG, we extracted protein and subjected to immunoblotting for apoptosis or autophagy related proteins. Results: We constructed compound-target network of RG and identified potential pathways related to HCC. RG inhibited growth of HCC through acceleration of cytotoxicity and reduction of wound healing ability of HCC. RG also increased apoptosis and autophagy through AMPK induction. In addition, its ingredients, 20S-PPD (protopanaxadiol) and 20S-PPT (protopanaxatriol), also induced AMPK mediated apoptosis and autophagy. Conclusion: RG effectively inhibited growth of HCC cells inducing apoptosis and autophagy via ATG/AMPK in HCC cells. Overall, our study suggests possibility as new anti-cancer drug on HCC by proof for the mechanism of the anti-cancer action of RG.

• Journal of Convergence Korean Medicine
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• v.6 no.1
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• pp.29-36
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• 2024

Objectives: Psoriasis is a common chronic inflammatory skin disease characterized by keratinocyte hyperproliferation and an excessive inflammatory response. Agents that can attenuate keratinocyte hyperproliferation and excessive inflammatory responses are considered potentially useful for the treatment of psoriasis. Daehwangmokdanpitang (DHMDPT) exhibits a broad range of bioactivities, including anti-proliferative and anti-inflammatory effects. This study aims to evaluate the anti-psoriatic potential of DHMDPT in vitro. Methods: HaCaT keratinocytes were stimulated with a mixture of IL-17A, IL-22, oncostatin M, IL-1α, and TNF-α (M5) to establish an in vitro psoriatic keratinocyte model. Cell viability was measured using the MTT assay. Quantitative real-time PCR (qRT-PCR) was performed to measure the mRNA levels of the hyperproliferative marker gene keratin 6 (KRT6) and inflammatory factors such as IL-6, TNF-α, and IL-23A. Additionally, chemokines including CCL5, CCL2, CCL20, and CXCL1 were measured by qRT-PCR. Results: DHMDPT attenuated M5-induced hyperproliferation, as indicated by a reduction in KRT6 expression in HaCaT keratinocytes. M5 stimulation significantly upregulated the mRNA levels of IL-6, TNF-α, and IL-23A. However, DHMDPT treatment attenuated the upregulation of IL-6 but not TNF-α or IL-23A. Additionally, DHMDPT inhibited the expression of CCL5, CCL2, and CXCL1, but not CCL20. Conclusion: DHMDPT effectively attenuated the M5-induced proliferation and inflammatory response in HaCaT keratinocytes. Therefore, DHMDPT could be an attractive candidate for future development as an anti-psoriatic agent.

• Nuclear Engineering and Technology
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• v.56 no.5
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• pp.1803-1812
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• 2024

The attractive properties of gadolinium-based nanoparticles as a positive contrast agent for magnetic resonance imaging (MRI) have piqued the interest of both researchers and clinicians. Nonetheless, due to the biotoxicity of gadolinium (III) ions' free radicals, there is a need to address this issue. Therefore, this research aimed to develop a biocompatible, dispersible, stable, hydrophilic, and less toxic cellulose nanocrystals/gadolinium oxide nanocomposite as contrast agent properties for MRI purposes. This study aimed to synthesize gadolinium oxide nanoparticles coated with cellulose nanocrystals with polyethylene glycol and sodium hydroxide (CNCs-PEG/NaOH)/Gd₂O₃ using the gamma irradiation method to reduce the particle size. The results showed that using a gamma irradiation dose of 10 kGy, quasi-spherical morphology with a size of approximately 5.5 ± 0.65 nm could be produced. Furthermore, the cytocompatibility of (CNCs-PEG/NaOH)/Gd₂O₃ nanocomposite synthesized was assessed through MTT assay tests on Hep G2 cells, which demonstrated good cytocompatibility without any cytotoxic effects within a concentration range of (10 ㎍/mL - 150 ㎍/mL) and had sufficient cellular uptake. Moreover, the T₁-weighted MRI of (CNCs-PEG/NaOH)/Gd₂O₃ nanocomposite revealed promising results as a positive contrast agent. It is envisaged that the gamma irradiation method is promising in synthesizing (CNCs-PEG/NaOH)/Gd₂O₃ nanocomposite with nanoscale for different applications, especially in the radiotherapy field.