Kim, Ro-Sa;Lee, Chang-Hoon;Lee, Jin-Moo;Cho, Jung-Hoon;Jang, Jun-Bock;Lee, Kyung-Sub
The Journal of Korean Obstetrics and Gynecology
/
v.22
no.2
/
pp.119-131
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2009
Purpose: The depression accompanied with menopuase shows the relation with the dopamine secretion. These studies were undertaken to evaluate the anti- oxidative and neuroprotective effects of Bunsimgieum(BSGE) on dopaminergic neurons. Methods: To estimate the antioxidant effects, we carried out 1.1-diphenyl-2- picrylhydrazyl (DPPH) free radical scavenging assay, 2,2'-azinobis-(3-ethylbenzothiazoline -6-sulfonic acid (ABTS) radical cation decolorization assay, and measurement of total polyphenolic content. To evaluate neuroprotective effect of BSGE in vitro, We performed thiazolyl blue tetrazolium bromide (MTT) assay, reactive oxygen species (ROS) creation in SH-SY5Y. Tyrosine hydroxylase (TH) immunocytochemistry, nitric oxide (NO) assay, and TNF-${\alpha}$ assay in primary rat mesencephalic dopaminergic neurons. Results: The DPPH free radical and the ABTS radical cation inhibition activities were increased at a dose dependent manner. Total polyphenolic content was 0.83%. In SH-SY5Y culture, BSGE significantly increased the decreased cell viability by 6-OHDA at the concentrations of 10${\mu}$g/m${\ell}$ in pre-treatment group, 0.1-200${\mu}$g/m${\ell}$ in post-treatment group. The production of ROS induced by 6-OHDA was significantly inhibited in BSGE treated group. In mesencephalic dopaminergic cell culture, the BSGE group reduced the dopaminergic cell loss against 6-OHDA toxicity and the production of No and TNF-${\alpha}$ at the concentration of 5${\mu}$g/m${\ell}$. Conclusion: These results shows that BSGE has antioxidant and neuroprotective effects in the dopaminergic cells through decreasing the production of ROS, NO and TNF-${\alpha}$ which can cause many neurodegenerative changes in brain cell. We suggest that BSGE could be useful for the treatment of postmenopausal depression related with the decrease of dopamine.
Fisetin is a bioactive flavonol molecule and has been shown to have antioxidant potential, but its efficacy has not been fully validated. The aim of the present study was to investigate the protective efficacy of fisetin on C2C12 murine myoblastjdusts under hydrogen peroxide (H2O2)-induced oxidative damage. The results revealed that fisetin significantly weakened H2O2-induced cell viability inhibition and DNA damage while blocking reactive oxygen species (ROS) generation. Fisetin also significantly alleviated cell cycle arrest by H2O2 treatment through by reversing the upregulation of p21WAF1/CIP1 expression and the downregulation of cyclin A and B levels. In addition, fisetin significantly blocked apoptosis induced by H2O2 through increasing the Bcl-2/Bax ratio and attenuating mitochondrial damage, which was accompanied by inactivation of caspase-3 and suppression of poly(ADP-ribose) polymerase cleavage. Furthermore, fisetin-induced nuclear translocation and phosphorylation of Nrf2 were related to the increased expression and activation of heme oxygenase-1 (HO-1) in H2O2-stimulated C2C12 myoblasts. However, the protective efficacy of fisetin on H2O2-mediated cytotoxicity, including cell cycle arrest, apoptosis and mitochondrial dysfunction, were greatly offset when HO-1 activity was artificially inhibited. Therefore, our results indicate that fisetin as an Nrf2 activator effectively abrogated oxidative stress-mediated damage in C2C12 myoblasts.
Objective: Liver fibrosis is a highly conserved wound-healing response and the final common pathway of chronic inflammatory injury. This study aimed to evaluate the potential anti-fibrotic effect of the combination of Rhei Radix et Rhizoma water extract (RW) and silymarin in a thioacetamide (TAA)-induced liver fibrosis model. Methods: The liver fibrosis mouse model was established through the intraperitoneal injection of TAA (1 week 100 mg/kg, 2-3 weeks 200 mg/kg, 4-8 weeks 400 mg/kg) three times per week for eight weeks. Animal experiments were conducted in five groups; Normal, Control (TAA-induced liver fibrosis mice), Sily (silymarin 50 mg/kg), RSL (RW 50 mg/kg+silymarin 50 mg/kg), and RSH (RW 100 mg/kg+silymarin 50 mg/kg). Biochemical analyses were measured in serum, including aspartate aminotransferase (AST), alanine aminotransferase (ALT), malondialdehyde (MDA), and ammonia levels. Liver inflammatory cytokines and fibrous biomarkers were measured by Western blot analysis, and liver histopathology was evaluated through tissue staining. Results: A significant decrease in the liver function markers AST and ALT and a reduction in ammonia and total bilirubin were observed in the group treated with RSL and RSH. Measurement of reactive oxygen species and MDA revealed a significant decrease in the RSL and RSH administration group compared to the TAA induction group. The expression of extracellular matrix-related proteins, such as transforming growth factor β1, α-smooth muscle actin, and collagen type I alpha 1, was likewise significantly decreased. All drug-administered groups had increased matrix metalloproteinase-9 but a decreasing tissue inhibitor of matrix metalloproteinase-1. RSL and RSH exerted a significant upregulation of NADPH oxidase 2, p22phox, and p47phox, which are oxidative stress-related factors. Furthermore, pro-inflammatory proteins such as cyclooxygenase 2 and interleukin-1β were markedly suppressed through the inhibition of nuclear factor kappa B activation. Conclusions: The administration of RW and silymarin suppressed the NADPH oxidase factor protein level and showed a tendency to reduce inflammation-related enzymes. These results suggest that the combined administration of RW and silymarin improves acute liver injury induced by TAA.
This study tried to examine the characteristics of attention deficits in patients with Obstructive Sleep Apenea(OSA) with different age levels, and to examine which indices of polysomnograms might be related to the indices of attention deficits in OSAs. Two age-level groups and a normal control group were subjected to two computerized attention tests, including a continuous performance test(CPT) and a change blindness task(CBT). In addition, the three groups were subjected to a Polysomnography to extract several sub-indicators of polysomnogram, and an Epworth Sleepiness Scale which measures subjective sleepiness. As results, the OSAs showed significantly more omission and commission errors in CPT, and they showed lower accuracy in CBT compared to the normal group. The results of a correlational analysis showed that attention deficits in OSA are significantly correlated with arterial oxygen saturation among sub-indicators of polysomnograms. In conclusion, OSAs seems to be less attentive, having difficulties in response inhibition, and having deficiencies in noticing important environmental changes. Age seems to make these deficiencies even worse. Especially, the relationship between attention deficiency and hypoxia which could cause irreversible cerebrum damage has an implication in cognitive impairment prevention through early treatment.
Lespedeza cuneata (LC) is a perennial plant used in herbal medicine to treat numerous diseases, including prostatic hyperplasia, diabetes, early atherosclerosis, and hematuria. Reference collections of bioactive compounds of LC are crucial for the determination of their pharmacological properties. However, little is known regarding its anti-oxidative and anti-inflammatory effects in alveolar macrophage (MH-S) cells. This study examined whether LC can inhibit reactive oxygen species and Coal fly ash (CFA) induced inflammation in MH-S cells. The anti-oxidative effects of LC were evaluated using 1,1-diphenyl-2-picrylhydrazyl (DPPH) and 2,2'-azino-bis(3-ethylbenzothiazoline-6-sulfonic acid) (ABTS) assays, anti-inflammatory effects were examined using nitric oxide (NO) assay, and cytotoxicity was analyzed using methyl thiazolyl tetrazolium assay. The expression of inflammatory cytokine genes was assessed through a reverse-transcription polymerase chain reaction. Our results revealed that LC exhibited high radical scavenging activity and a dose-dependent (7.8-1,000 ㎍/mL) inhibition of oxidation as compared to ascorbic acid and Trolox. It also inhibited CFA-induced NO production in MH-S cells. Moreover, it suppressed the CFA exposure-mediated expression of pro-inflammatory mediators and cytokines, including inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), interleukin (IL)-1β, IL-6, and tumor necrosis factor-α. These results suggest that LC is a potent antioxidant and anti-inflammatory agent that can be useful as a nutraceutical product.
Background: Ginsenoside Rg1 (Rg1) is one of the main active components in Chinese medicines, Panax ginseng and Panax notoginseng. Research has shown that Rg1 has a protective effect on the cardiovascular system, including anti-myocardial ischemia-reperfusion injury, anti-apoptosis, and promotion of myocardial angiogenesis, suggesting it a potential cardiovascular agent. However, the protective mechanism involved is still not fully understood. Methods: Based on network pharmacology, ligand-based protein docking, proteomics, Western blot, protein recombination and spectroscopic analysis (UV-Vis and fluorescence spectra) techniques, potential targets and pathways for Rg1 against myocardial ischemia (MI) were screened and explored. Results: An important target set containing 19 proteins was constructed. Two target proteins with more favorable binding activity for Rg1 against MI were further identified by molecular docking, including mitogen-activated protein kinase 1 (MAPK1) and adenosine kinase (ADK). Meanwhile, Rg1 intervention on H9c2 cells injured by H2O2 showed an inhibitory oxidative phosphorylation (OXPHOS) pathway. The inhibition of Rg1 on MAPK1 and OXPHOS pathway was confirmed by Western blot assay. By protein recombination and spectroscopic analysis, the binding reaction between ADK and Rg1 was also evaluated. Conclusion: Rg1 can effectively alleviate cardiomyocytes oxidative stress injury via targeting MAPK1 and ADK, and inhibiting oxidative phosphorylation (OXPHOS) pathway. The present study provides scientific basis for the clinical application of the natural active ingredient, Rg1, and also gives rise to a methodological reference to the searching of action targets and pathways of other natural active ingredients.
Jinshun Zhan;Zhiyong Gu;Haibo Wang;Yuhang Liu;Yanping Wu;Junhong Huo
Animal Bioscience
/
v.37
no.2
/
pp.303-314
/
2024
Objective: Rutin, also called vitamin P, is a flavonoids from plants. Previous studies have indicated that rutin can alleviate the injury of tissues and cells by inhibiting oxidative stress and ameliorating inflammation. There is no report on the protective effects of rutin on goat rumen epithelial cells (GRECs) at present. Hence, we investigated whether rutin can alleviate lipopolysaccharide (LPS)-induced damage in GRECs. Methods: GRECs were cultured in basal medium or basal medium containing 1 ㎍/mL LPS, or 1 ㎍/mL LPS and 20 ㎍/mL rutin. Six replicates were performed for each group. After 3-h culture, the GRECs were harvested to detect the relevant parameters. Results: Rutin significantly enhanced the cell activity (p<0.05) and transepithelial electrical resistance (TEER) (p<0.01) and significantly reduced the apoptosis rate (p<0.05) of LPS-induced GRECs. Rutin significantly increased superoxide dismutase, glutathione peroxidase, and catalase activity (p<0.01) and significantly decreased lactate dehydrogenase activity and reactive oxygen species and malondialdehyde (MDA) levels in LPS-induced GRECs (p<0.01). The mRNA and protein levels of interleukin 6 (IL-6), IL-1β, and C-X-C motif chemokine ligand 8 (CXCL8) and the mRNA level of tumor necrosis factor-α (TNF-α) and chemokine C-C motif ligand 5 (CCL5) were significantly increased in LPS-induced GRECs (p<0.05 or p<0.01), while rutin supplementation significantly decreased the mRNA and protein levels of IL-6, TNF-α, and CXCL8 in LPS-induced GRECs (p<0.05 or p<0.01). The mRNA level of toll-like receptor 2 (TLR2), and the mRNA and protein levels of TLR4 and nuclear factor κB (NF-κB) was significantly improved in LPS-induced GRECs (p<0.05 or p<0.01), whereas rutin supplementation could significantly reduce the mRNA and protein levels of TLR4 (p<0.05 or p<0.01). In addition, rutin had a tendency of decreasing the protein levels of CXCL6, NF-κB, and inhibitor of nuclear factor kappa-B alpha (0.05
Maheshkumar Prakash Patil;Yong-Suk Lee;Mi Jeong Jo;Yong Bae Seo;Gun-Do Kim
Journal of Life Science
/
v.34
no.9
/
pp.647-655
/
2024
The synthesis of cerium oxide nanoparticles (nanoceria, CeO2) has received significant attention across scientific and technological disciplines in the last decade. This article explores an overview of the green synthesis method and the antibacterial activity of nanoceria. The utilization of biological materials, such as plants and microorganisms, in the synthesis of nanoceria, has gained attention as an ecofriendly approach. Plants are rich in phytochemicals, including alkaloids, flavonoids, phenols, proteins, and other nutritious components. Likewise, microorganisms generate bioactive metabolites, pigments, enzymes, proteins, acids, and antibiotics. The phytochemicals and metabolites are involved in the reduction of metal salt into nanoceria and provide stability to synthesized nanoparticles. Nanoceria synthesis using plants and microorganisms is facile and ecofriendly, and synthesized nanoceria are biocompatible. Many biomedical applications of nanoceria have been reported, including those that are anticancer, anti-inflammatory, larvicidal, enzyme inhibiting, antibiofilm, and antimicrobial. However, in this review, we focused on and described in detail the antibacterial potential of nanoceria. The antibacterial activity of nanoceria occurs due to excessive reactive oxygen species generation, the impairment of the cell membrane, and the inhibition of cellular mechanisms. Ultimately, this review's primary goal is to provide readers with a logical understanding of the significant achievements of nanoceria as a cutting-edge therapeutic agent for treating a range of microbial pathogens and combating other diseases.
Objectives : This study was conducted to evaluate the cytotoxic protective effects of Jinsimyusaeng-hwan (Modified Ojayeonjong-hwan) against oxidative stress. Methods : 1,1-diphenyl-2-picrylhydrazyl (DPPH), 2,2'-azinobis-(3-ethyl-benzothiazoline-6-sulfonic acid)(ABTS) radical scavenging activity and ferric reducing ability of plasma (FRAP) method were used to estimate the antioxidant activity of Jinsimyusaeng-hwan. C2C12 myoblasts were used to reevaluate the antioxidant effects. And apoptosis analysis, mitochondrial membrane potential analysis, measurement of intracellular reactive oxygen species levels were conducted to investigate antioxidant activity of Jinsimyusaeng-hwan. Results : In comparison of DPPH free radical and ABTS cationic radical scavenging activity, it increased as the concentration of water extracts of Jinsimyusaeng-hwan(WEJ) and 70% ethanol extracts of Jinsimyusaeng-hwan (EEJ) increased. In the results of comparing the total phenol content and reducing power using the FRAP method, extracts with high total phenol content also showed high reducing power. In comparison of the protective effect against H2O2-induced oxidative stress in C2C12 myoblasts, WEJ had no significant effect, but the EEJ inhibited H2O2-mediated cytotoxicity in a concentration-dependent manner. The cytotoxic protective effect of EEJ against oxidative stress in C2C12 myoblasts was correlated with their inhibitory effects on H2O2-induced apoptosis and cell cycle arrest. In H2O2-treated C2C12 myoblasts, the apoptosis inhibitory effects of EEJ were associated with suppression of mitochondrial dysfunction and DNA damage. The protective effect of EEJ against H2O2-induced oxidative stress in C2C12 myoblasts were directly related to the inhibition of ROS generation. Conclusion : Jinsimyusaeng-hwan extracts have cytotoxic protective effects against oxidative stress, and it was better in 70% ethanol extract than in water extract.
Park, Eun Hye;Lee, Hyo Jung;Lee, Soo Yeon;Kim, Sun Young;Yi, Ho Keun;Lee, Dae Yeol;Hwang, Pyoung Han
Clinical and Experimental Pediatrics
/
v.52
no.2
/
pp.213-219
/
2009
Purpose:Iron is a critical nutritional element that is essential for a variety of important biological processes, including cell growth and differentiation, electron transfer reactions, and oxygen transport, activation, and detoxification. Iron is also required for neoplastic cell growth due to its catalytic effects on the formation of hydroxyl radicals, suppression of host defense cell activities, and promotion of cancer cell multiplication. Chronic transfusion-dependent patients receiving chemotherapy may have iron overload, which requires iron-chelating therapy. We performed this study to demonstrate whether the iron chelating agent deferoxamine induces apoptosis in Saos-2 osteosarcoma cells, and to investigate the underlying apoptotic mechanism. Methods:To analyze the apoptotic effects of an iron chelator, cultured Saos-2 cells were treated with deferoxamine. We analyzed cell survival by trypan blue and crystal violet analysis, apoptosis by nuclear condensation, DNA fragmentation, and cell cycle analysis, and the expression of apoptotic related proteins by Western immunoblot analysis. Results:Deferoxamine inhibited the growth of Saos-2 cell in a time- and dose-dependent manner. The major mechanism for growth inhibition with the deferoxamine treatment was by the induction of apoptosis, which was supported by nuclear staining, DNA fragmentation analysis, and flow cytometric analysis. Furthermore, bcl-2 expression decreased, while bax, caspase-3, caspase-9, and PARP expression increased in Saos-2 cells treated with deferoxamine. Conclusion:These results demonstrated that the iron chelating agent deferoxamine induced growth inhibition and mitochondrial-dependent apoptosis in osteosarcoma Saos-2 cells, suggesting that iron chelating agents used in controlling neoplastic cell fate can be potentially developed as an adjuvant agent enhancing the anti-tumor effect for the treatment of osteosarcoma.
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