The susceptibilities of aldehyde dehydrogenase (AldDH) and alcohol dehydrogenase (ADH) to active oxygen generated by xanthine-xanthine oxidase (XOD) system were studied. Incubation of AldDH with 2$\times$10$^{-3}$ units of XOD for 30 min at $25^{\circ}C$ resulted in the decrease of enzyme activity to 30% and it was inactivated completely when incubated with 5$\times$10$^{-3}$ units of XOD. Whereas 70% of ADH activity was retained after exposure to 5$\times$10$^{-3}$ units of XOD for 30 min, 40% of ADH activity was retained after exposure to 5$\times$10$^{-2}$ unit of XOD for 30 min. This inhibition effect by the active oxygen was preventable by catalase and glutathione, but not by SOD. The rates of the NADPH-dependent oxygen consumption by the liver S-9 mixture and microsomes were also determined in this study. Rate of oxygen consumption is increased in the liver S-9 mix and microsomes from phenobarbital-treated rat, and it was consistent with increased lipid peroxidation. In the presense of ethanol as a substrate, the oxygen consumption rates were increased. It is reported that hepatic AldDH activity is depressed in alcoholic liver diseases, however there is few report that explains the reason of depressed AldDH activity. These results are supportive of the theory that the increase in hepatic ethanol oxidation through the induced ME activity after chronic ethanol feeding generate oxygen radical at elevated rates and it leads to the depression of AldDH activity.
The purpose of this study is to investigate the anti-aging and anti-oxidative effects of oral administration with SYG (SipYiMiGwanJungTang) decoction in early aged rats. The results were as follows : 1. At the 52 week of the SYG group, the body weight gain was decreased. 2. At the 52 week of the SYG group, the activity of the SOD in the liver was significantly increased than the 10, 22 and 40 week. 3. At the 52 week of the SYG group, the level of the glutathione in the liver was significantly increased than the normal group. 4. At the 68 week of the SYG group, the activity of the catalase in the liver was significantly increased than the normal and control group. 5. At the 52 week of the normal group, the level of the NO in the liver was significantly increased than the 22 and 40 weeks. But, the level of the NO of the SYG group was not changed by the aging. 6. At the 52 and 68 weeks of the SYG group, the level of the MDA in the liver was significantly decreased than the normal and control groups. These results suggest that oral administration of SYG (SipYiMiGwanJungTang) decoction has anti-oxidative and anti-aging effects in early aged rats.
Effects of Ramaria botrytis methanol extract on hepatotoxicity in $benzo({\alpha})pyrene(B({\alpha})P)-treated$ mice were investigated. R. botrytis methanol extract was intraperitioneally injected once a day for successive 5 days, followed by treatment with $B({\alpha})P$ on the fifth day. Antioxidant activities of R. botrytis methanol extract were examined by measuring the free radical-scavenging effect on 1,1-diphenyl-2-picrylhydrazyl (DPPH) radical. In DPPH method, R. botrytis methanol extract showed strong antioxidative activies. The increased activities of superoxide dismutase, catalase, and glutathione peroxidase after $B({\alpha})P-treatment$ were decreased by treatment of R. botrytis methanol extract. Glutathione content and glutathione S-transferase activity depleted by $B({\alpha})P$ were significantly increased, but elevation of lipid peroxide content induced by $B({\alpha})P$ was decreased by R. botrytis methanol extract. These results suggest that R. botrytis methanol extract is believe to be a possible protective effect against $B(\alpha)P-induced$ hepatotoxicity in mice.
Jo, Jin Ha;Bae, Eun Young;Lee, Tae Kyoung;Kim, Myung Hyun;Lee, Seung Woong;Kim, Byoung Soo;Lim, Chi Hwan
Korean Journal of Medicinal Crop Science
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v.24
no.2
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pp.152-158
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2016
Background: Sanguisorba officinalis has been used in traditional Asian medicine owing to its beneficial effects on various diseases. The purpose of this study was to evaluate the effect of S. officinalis on the antioxidant system of Streptozotocin (STZ) and Alloxan (ALL) induced diabetic rats. Methods and Results: Triglyceride and Low-Density Lipoprotein (LDL)-cholesterol levels decreased in the STZ-induced diabetic groups treated with S. officinalis extract (SOE) compared to the corresponding levels in the control groups. Moreover, in the ALL-induced diabetic groups, SOE reduced triglyceride, LDL-cholesterol, and High-Density Lipoprotein (HDL)-cholesterol levels. Malondialdehyde (MDA) levels decreased significantly in the STZ and ALL-induced groups treated with SOE compared to the corresponding levels in the control group. Further, Glutathione (GSH) levels increased but did not reach statistical significance. The levels of Superoxide Dismutase (SOD) and Glutathione-S-Transferase (GST) showed a tendency to recover with SOE treatment in the STZ and ALL-induced diabetic groups. In addition, Catalase (CAT) levels in the SOE treatment group decreased significantly compared to those in the control group. Conclusions: These results suggest that SOE might be an effective agent in attenuating oxidative stress in diabetic patients by improving blood lipid profiles and inducing the anti-oxidative enzyme systems.
To investigate the antioxidative effects of an etbylacetate fraction extracted from the flowers of Chrysanthemum indicum L. (Chrysanthemi Flos) on the antioxidative system and lipid profiles of rats with ethanol induced hepatotoxicity. Sprague-Dawley rats weighing $100\~150$ g were divided into 5 groups: normal group (NOR), Chrysanthemi Flos EtOAC fraction (200 mg/kg) treated group (S1), $35\%$ etbanol (10 mL/kg) treated group (S2), Chrysanthemi Flos EtOAC fraction (200 mg/kg) and ethanol concomitantly treated group (S3) and Chrysanthemi Flos EtOAC fraction (400 mg/kg) and ethanol concomitantly treated group (S4), respectively. The antioxidative activity of each fraction was decreased in order of EtOAC, n-hexane, n-BuOH, water and chloroform. The growth rates and feed efficiency ratios were decreased by ethanol treatment, but were gradually restored to similar levels as in the NOR group by administering Chrysanthemi Flos EtOAC fraction. The whole blood concentrations of total cholesterol and LDL-cholesterol, and the activities of ALT and AST that were elevated by ethanol were significantly decreased in the Chrysanthemi Flos EtOAC fraction treated groups. It was also observed that the activities of SOD, catalase, xanthine oxidase and GSH-Px elevated by ethanol in rat liver were markedly decreased in the Chrysanthemi Flos EtOAC fraction treated group as compared to S2. These results suggest that Chrysanthemi Flos EtOAC fraction has possible protective effects against ethanol induced hepatotoxicity in rat liver.
Fractional solvent extraction by organic solvents such as hexane, chloroform, ethylacetate, and butanol was carried out using 70% ethanol extract of apple flower leaves. Biological activities including antioxidant, whitening, antimicrobial and anti-wrinkle activities were investigated and bio-active materials of the extracts were identified using GC/MSD. Among the tested solvent fractions, ethylacetate fraction showed the highest total polyphenol content (1218.94 ${\mu}g/mL$), and flavonoid (140 ${\mu}g/mL$). The DPPH radical scavenging activities was over 80% at a dry matterbased concentration of 200 ${\mu}g/{\mu}L$ and SOD-like activity was over 90% at 50 ${\mu}g/mL$ concentration in ethylacetate fraction that was slightly lower than of ascorbic aicd. Tyrosinase inhibition activity related to skin-whitening was over 60% by ethylacetate fraction of 100 ${\mu}g/mL$. As an anti-aging effect, elastase inhibitory activity was about 45% in ethylacetate fraction. Also, it showed a significantly antimicrobial activity against P. acenes. From GC/MSD analysis, a characteristic peak of high content in ethylacetate fraction was identified as kaempferol, which has been reported as a bioactive compound.
Objectives: The aim of this study was to investigate the anti-inflammatory effects of Curcuma longa rhizoma extract in an experimental rat model of osteoarthritis. Methods: Osteoarthritis was induced in rats by injecting monosodium iodoacetate (MIA) into the knee joint cavity of rats. The rats were divided into 5 groups (Normal, Control, positive comparison, low (CL) and high (CH) concentration groups). Rats in the low concentration (CL) group had MIA-induced osteoarthritis; they were treated with Curcuma longa rhizoma extract at a dose of 50mg/kg body weight. Rats in the high concentration (CH) group had MIA-induced osteoarthritis; they were treated with Curcuma longa rhizoma extract at a dose of 100mg/kg body weight. Hind paw weight distribution and ROS levels were measured. At the end of all treatments, changes in alanine aminotransferase (ALT), aspartate aminotransferase (AST), blood urea nitrogen (BUN), and creatinine levels were analyzed. In addition, inflammatory protein levels were evaluated by western blot analysis. Results: In this study, hind paw weight distribution significantly improved in the CL and CH groups, while. Reactive oxygen species (ROS) production significantly decreased in both. The levels of ALT, AST, BUN, and creatinine did not significantly change in either group. The production of nicotinamide adenine dinucleotide phosphate oxidase 4 (NOX4), $p47^{phox}$, and Ras-related C3 botulinum toxin substrate 1 (RAC1) decreased in both. Catalase, heme oxygenase-1 (HO-1) and superoxide dismutase (SOD) significantly increased in the CL and CH groups, respectively. Nuclear factor erythroid 2 (Nrf2) increased, but there were no significant differences between the experimental and control groups. Inflammatory cytokines, including nuclear factor-kappa Bp65 (NF-${\kappa}Bp65$), interleukin-1beta (IL-$1{\beta}$), and tumor necrosis factor-alpha (TNF-${\alpha}$), decreased significantly in both the CL and CH groups. Conclusions: Our results showed that Curcuma longa rhizoma extract has anti-inflammatory effects. Anti-inflammatory activity is regulated by the inhibition of inflammatory cytokines and mediators, such as NF-${\kappa}B$, therefore, it suppresses cartilage damage as well.
Sevoflurane postconditioning (SPostC) has been proved effective in cardioprotection against myocardial ischemia/reperfusion injury. It was also reported that heat shock protein 70 (HSP70) could be induced by sevoflurane, which played a crucial role in hypoxic/reoxygenation (HR) injury of cardiomyocytes. However, the mechanism by which sevoflurane protects cardiomyocytes via HSP70 is still not understood. Here, we aimed to investigate the related mechanisms of SPostC inducing HSP70 expression to reduce the HR injury of cardiomyocytes. After the HR cardiomyocytes model was established, the cells transfected with siRNA for HSP70 (siHSP70) or not were treated with sevoflurane during reoxygenation. The lactate dehydrogenase (LDH) level was detected by colorimetry while cell viability and apoptosis were detected by MTT and flow cytometry. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and Western blotting were used to detect HSP70, apoptosis-, cell cycle-associated factors, iNOS, and Cox-2 expressions. Enzyme-linked immuno sorbent assay (ELISA) was used to measure malondialdehyde (MDA) and superoxide dismutase (SOD). SPostC decreased apoptosis, cell injury, oxidative stress and inflammation and increased viability of HR-induced cardiomyocytes. In addition, SPostC downregulated Bax and cleaved caspase-3 levels, while SPostC upregulated Bcl-2, CDK-4, Cyclin D1, and HSP70 levels. SiHSP70 had the opposite effect that SPostC had on HR-induced cardiomyocytes. Moreover, siHSP70 further reversed the effect of SPostC on apoptosis, cell injury, oxidative stress, inflammation, viability and the expressions of HSP70, apoptosis-, and cell cycle-associated factors in HR-induced cardiomyocytes. In conclusion, this study demonstrates that SPostC can reduce the HR injury of cardiomyocytes by inducing HSP70 expression.
International Journal of Internet, Broadcasting and Communication
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v.13
no.2
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pp.145-155
/
2021
With the recent rapid improvement in the standards of life and westernization of dietary lifestyles, the consumption of high-calorie diets such as high-fat and high-protein red meat and instant foods has increased, while less vegetables containing dietary fiber are consumed. In addition to that, stress, erroneous dietary behaviors, and contaminated environments are linked to the risk of developing ulcerative colitis, which is on the rise. Another cause of ulcerative colitis is that involve laxative abuse, including repeated, frequent use of laxatives, and include such conditions as deteriorated bowel function, irritable bowel syndrome, diarrhea, intestinal inflammation, etc. The present study aimed to investigate the comparative evaluation of pharmacological efficacy between sulfasalazine alone and combination with herbal medicine on dextran sodium sulfate (DSS)-induced UC in mice. Balb/c mice received 5% DSS in drinking water for 7 days to induce colitis. Animals were divided into five groups (n = 9): group I-normal group, group II-DSS control group, group III-DSS + sulfasalazine (30 mg/kg), group IV-DSS + sulfasalazine (60 mg/kg), group V-DSS + sulfasalazine (30 mg/kg) + Radish Extract mixture (30 mg /kg) (SRE). DSS-treated mice developed symptoms similar to those of human UC, such as severe bloody diarrhea and weight loss. SRE supplementation, as well as sulfasalazine, suppressed colonic length and mucosal inflammatory infiltration. In addition, SRE treatment significantly reduced the expression of pro-inflammatory signaling molecules through suppression both mitogen-activated protein kinases (MAPK) and nuclear factor-kappa B (NF-κB) signaling pathways, and prevented the apoptosis of colon. Moreover, SRE administration significantly led to the up-regulation of antioxidant enzyme including SOD and Catalase. This is the first report that Radish extract mixture combined with sulfasalazine protects against experimental UC via the inhibition of both inflammation and apoptosis, very similar to the standard-of-care sulfasalazine.
Hongming Lv;Yvxi He;Jingjing Wu; Li Zhen ;Yvwei Zheng
Journal of Veterinary Science
/
v.24
no.1
/
pp.2.1-2.14
/
2023
Background: Hypothermia is a crucial environmental factor that elevates the risk of cardiovascular disease, but the underlying effect is unclear. Objectives: This study examined the role of cold stress (CS) in cardiac injury and its underlying mechanisms. Methods: In this study, a chronic CS-induced myocardial injury model was used; mice were subjected to chronic CS (4℃) for three hours per day for three weeks. Results: CS could result in myocardial injury by inducing the levels of heat shock proteins 70 (HSP70), enhancing the generation of creatine phosphokinase-isoenzyme (CKMB) and malondialdehyde (MDA), increasing the contents of tumor necrosis factor-α (TNF-α), high mobility group box 1 (HMGB1) interleukin1b (IL-1β), IL-18, IL-6, and triggering the depletion of superoxide dismutase (SOD), catalase (CAT), and glutathione (GSH). Multiple signaling pathways were activated by cold exposure, including pyroptosis-associated NOD-like receptor 3 (NLRP3)-regulated caspase-1-dependent/Gasdermin D (GSDMD), inflammation-related toll-like receptor 4 (TLR4)/myeloid differentiation factor 88 (MyD88)-mediated nuclear factor kappa B (NF-κB), and mitogen-activated protein kinase (MAPK), as well as oxidative stressinvolved thioredoxin-1/thioredoxin-interacting protein (Txnip) signaling pathways, which play a pivotal role in myocardial injury resulting from hypothermia. Conclusions: These findings provide new insights into the increased risk of cardiovascular disease at extremely low temperatures.
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