Sublethal dose of bacterial lipopolysaccharide (LPS) would induce protection against cardiac ischemic/reperfusion (I/R) injury. This study examines the following areas: 1) the temporal induction of the cardio-protection produced by LPS; and 2) the relations between a degree of protection and the myocardial prostacyclin ($PGI_2$) production. Rats were administered LPS (2 mg/kg, i.v.), and hearts were removed 1, 4, 8, 14, 24, 48, 72,and 96 h later. Using Langendorff apparatus, haemodynamic differences during 25 min of global ischemia/30 min reperfusion were investigated. The concentration of $PGI_2$ in aliquots of the coronary effluent was determined by radioimmunoassay as its stable hydrolysis product $6-keto-PGF1_{\alpha}$ and lactate dehydrogenase release were measured as an indicative of cellular injury. LPS-induced cardiac protection against I/R injury appeared 4 h after LPS treatment and remained until 96 h after treatment. $PGI_2$ release increased 2-3 fold at the beginning of reperfusion compared to basal level except in hearts treated with LPS for 48 and 72 h. In hearts removed 48 and 72 h after LPS treatment, basal $PGI_2$ was increased. To determine the enzymatic step in relation to LPS-induced basal $PGI_2$ production, we examined prostaglandin H synthase (PGHS) protein expression, a rate limiting enzyme of prostaglandin production, by using Western blot analysis. LPS increased PGHS protein expression in hearts at 24, 48, 72, 96 h after LPS treatment. Induction of PGHS expression appeared in both isotypes of PGHS, a constitutive PGHS-1 and an inducible PGHS-2. To identify the correlationship between $PGI_2$ production and the cardioprotective effect against I/R injury, indomethacin was administered in vivo or in vitro. Indomethacin did not inhibit LPS-induced cardioprotection, which was not affected by the duration of LPS treatment. Taken together, our results suggest that $PGI_2$ might not be the major endogenous mediator of LPS-induced cardioprotection.
In recent decades, titanium dioxide ($TiO_2$) nanoparticles have been used in various applications, including paints, coatings, and food. However, data are lacking on the toxicological aspects associated with their use. The aim of this study was to assess the inhalation toxicity of $TiO_2$ nanoparticles in rats by using inhalation exposure. Male Wistar rats were exposed to $TiO_2$ nanoparticles for 2 weeks (6 hr/day, 5 days/week) at a mean mass concentration of $11.39{\pm}0.31mg/m^3$. We performed time-course necropsies at 1, 7, and 15 days after exposure. Lung inflammation and injury were assessed on the basis of the total and individual cell counts in bronchoalveolar lavage fluid (BALF), and by biochemical assays, including an assay for lactate dehydrogenase (LDH). Furthermore, histopathological examination was performed to investigate the lungs and nasal cavity of rats. There were no statistically significant changes in the number of BALF cells, results of biochemical assays of BALF and serum, and results of cytokine analysis. However, we did observe histopathological changes in the nasal cavity tissue. Lesions were observed at post-exposure days 1 and 7, which resolved at post-exposure day 15. We also calculated the actual amounts of $TiO_2$ nanoparticles inhaled by the rats. The results showed that the degree of toxicity induced by $TiO_2$ nanoparticles correlated with the delivered quantities. In particular, exposure to small particles with a size of approximately 20 nm resulted in toxicity, even if the total particle number was relatively low.
Objective: In the present study, we investigated the protective effects of low-intensity treadmill training in doxorubicin-induced cardiotoxicity rat models. Design: Randomized controlled trial. Methods: In this study, we randomly divided them into four groups. The normal group included non-cardiotoxicity normal control (n=10), the control group included non-treadmill training after doxorubicin-induced cardiotoxicity (n=10), the experimental group I included low-intensity treadmill training (3 m/min) after doxorubicin-induced cardiotoxicity (n=10), and the experimental group II included low-intensity treadmill training (8 m/min) after doxorubicin-induced cardiotoxicity (n=10). Rats in the treadmill training group underwent treadmill training, which began at 2 weeks after first intraperitoneal injection. We determined the body weight change for each rat on days 1 and 21. Biochemical markers (lactate dehydrogenase [LDH], creatine kinase [CK], glutathion, aspartate transaminase [AST], and alanine transaminase [ALT]) concentration in the serum change of rats from all four groups was examined at the end of the experiment. Results: The results showed that the experimental group I and II showed a significant increase in body weight as compared with that of the control group (p<0.05). We observed that the biochemical markers (LDH, CK, glutathion, AST, and ALT) were improved in the experimental group I than the experimental group II (p<0.05). There was no difference between the experimental groups. Conclusions: In conclusion, our data suggest that low-intensity treadmill training applied after doxorubicin treatment protects against cardiotoxicity following treatment, possibly by enhancing antioxidant defenses and inhibiting cardiac muscle cell apoptosis.
Kim, Sung-Hwa;Cheon, Ho-Jun;Park, Jin-Gu;Kim, Yeong-Sik;Kang, Sam-Sik;Xu, Guang-Hua;Lee, Seung-Ho;Son, Kun-Ho;Lee, Sun-Mi
YAKHAK HOEJI
/
v.50
no.6
/
pp.358-366
/
2006
The aim of this study was to investigate the protective effects of glycynhizin, active glycosides of Glycyrrhizae Radix, and baicalin, bioactive flavonoid isolated from Scutellariae Radix, on hepatocyte injury induced by carbon tetrachloride(CCl$_4$, 10 mM), tert-butyl hydroperoxide (TBH, 0.5 mM), and D-galactosamine (GaIN, 30 mM). Primary cultures of rat hepatocyte (18 hr cultured) were treated with CCl$_4$, TBH, or GaIN and various concentrations (0.1, 1, 10, and 100 ${\mu}$M) of glycyrrhizin or baicalin. Activity was accessed by determining the release of lactate dehydrogenase (LDH) and aminotransferses. CCl$_4$ significantly increased the levels of LDH, alanine aminotransferase (ALT), and aspartate aminotransferase(AST) and these increases were prevented by baicalin concentrations of 0.1,1, and 100 ${\mu}$M. The increases in ALT and AST levels were reduced by glycyrrhizin concentration of 100 ${\mu}$M. The level of LDH was markedly increased by TBH, and this increase was reduced by both glycyrrhizin and baicalin. ALT and AST levels were increased by TBH, which were prevented by glycynhizin and bacalin, respectively: GaIN markedly increased the levels of LDH, ALT and AST These increases was significantly reduced by both glycyrrhizin and baicalin. These results suggest that glycynhizin and baicalin possess the hepatoprotective activity.
Anwar, Ayaz;Siddiqui, Ruqaiyyah;Shah, Muhammad Raza;Khan, Naveed Ahmed
Journal of Microbiology and Biotechnology
/
v.29
no.1
/
pp.171-177
/
2019
Parasitic infections have remained a significant burden on human and animal health. In part, this is due to lack of clinically-approved, novel antimicrobials and a lack of interest by the pharmaceutical industry. An alternative approach is to modify existing clinically-approved drugs for efficient delivery formulations to ensure minimum inhibitory concentration is achieved at the target site. Nanotechnology offers the potential to enhance the therapeutic efficacy of drugs through modification of nanoparticles with ligands. Amphotericin B, nystatin, and fluconazole are clinically available drugs in the treatment of amoebal and fungal infections. These drugs were conjugated with gold nanoparticles. To characterize these gold-conjugated drug, atomic force microscopy, ultraviolet-visible spectrophotometry and Fourier transform infrared spectroscopy were performed. These drugs and their gold nanoconjugates were examined for antimicrobial activity against the protist pathogen, Acanthamoeba castellanii of the T4 genotype. Moreover, host cell cytotoxicity assays were accomplished. Cytotoxicity of these drugs and drug-conjugated gold nanoparticles was also determined by lactate dehydrogenase assay. Gold nanoparticles conjugation resulted in enhanced bioactivity of all three drugs with amphotericin B producing the most significant effects against Acanthamoeba castellanii (p < 0.05). In contrast, bare gold nanoparticles did not exhibit antimicrobial potency. Furthermore, amoebae treated with drugs-conjugated gold nanoparticles showed reduced cytotoxicity against HeLa cells. In this report, we demonstrated the use of nanotechnology to modify existing clinically-approved drugs and enhance their efficacy against pathogenic amoebae. Given the lack of development of novel drugs, this is a viable approach in the treatment of neglected diseases.
One hundred and forty-four cross-bred market pigs weighing approximately 110 kg were randomly divided into six groups in a 3 (duration of fasting prior to loading; 0, 12 and 24 h) ${\times}$ 2 (handling stress; minimal vs stimulated handling stress) factorial arrangement of treatments. The stimulated handling stress group received overally rough handling including electric prod stimulation during loading, transport and lairage at least once at each step. All the animals received 3-h lairage prior to slaughter. Blood and longissimus dorsi muscle (LM) samples were taken at slaughter and after overnight chilling of the carcass, respectively. Mean plasma glucose concentration, as expected, was less in the 12 h- or 24 h-fasting group than in the 0 h-fasting, whereas cortisol concentration was greater (P<0.05) in the 24 h- vs 0 h-fasting group. Plasma concentrations of stress indicators glucose, cortisol, creatine kinase and lactate dehydrogenase were greater in the stimulated vs minimal handling stress group. There were no interactions between the duration of fasting and handling stress in their effects on these blood variables. The incidence of pale, soft and exudative (PSE) carcass and drip loss of LM were reduced in the 12 h- or 24 h- vs 0 h-fasting group, whereas the 24-h postmortem LM pH and color including the lightness and redness were not affected by the duration of fasting. The incidence of PSE carcass and physicochemical characteristics of LM, however, were not changed by the stimulated vs minimal handling stress. In conclusion, results suggest that fasting the market pig overnight prior to transport is desirable in terms of reducing the incidence of PSE carcass. Rough handling of market pigs may not affect the carcass quality of the animals when an enough lairage time is provided. However, rough handling inflicts a stimulated stress on the animal, which is manifested by increased blood concentrations of stress indicators, and therefore should be avoided fer animal welfare.
This study was conducted to determine the effects of exogenous zinc-metallothionein (Zn-MT) on anti-oxidative function and pork quality. After feeding a corn-soybean meal-based diet for two weeks, 48 pigs ($Duroc{\times}Landrace{\times}Chinese\;Black Pig$) were assigned randomly to four groups. Pigs in Group 1 were maintained under non-stress conditions, whereas pigs in Groups 2, 3 and 4 were aggressively handled for 25 min to produce stress. Pigs in Groups 1, 2, 3, and 4 received intramuscular administration of saline (control group; CON), 0 (negative control group; NCON), 0.8 (low dose group; LOW), and 1.6 (high dose group; HIGH) mg rabbit liver Zn-MT per kg body weight, respectively. Pigs were slaughtered at 3 and 6 h post-injection. Zn-MT treatment increased (p<0.05) the activities of superoxide dismutase (SOD) and glutathione-peroxidase (GSH-PX) while decreasing the concentration of malondialdehyde (MDA) in liver. These responses were greater (p<0.05) at 6 h than at 3 h post Zn-MT injection. Zn-MT treatment increased (p<0.05) hepatic SOD mRNA levels in a time and dose-dependent manner and decreased (p<0.05) serum glutamate-pyruvate transaminase and lactate dehydrogenase activities (indicators of tissue integrity). Zn-MT administration decreased (p<0.05) lactate concentration and increased (p<0.05) pH and water-holding capacity in the longissimus thorasis meat. Collectively, our results indicate that intramuscular administration of Zn-MT to pre-slaughter stressed pigs improved tissue anti-oxidative ability and meat quality.
Proceedings of the Plant Resources Society of Korea Conference
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v.18
no.1
/
pp.52-60
/
2005
The objectives of present study were to investigate the hepatoprotective and antioxidative effects of onion extracts. Primary cultures of rat hepatocytes were incubated with 1.5 mM tert-butyl hydroperoxide(t-BHP), potent oxidizing agent for liver injury for 1 hr in the presence or absence of various concentrations (0, 0.01, 0.05, 0.1 or 0.3 mg/ml) of onion extract. Cytotoxicity and cell viability were determined by measuring glutamic oxaloacetic transaminase(GOT) activity, lactate dehydrogenase(LDH) activity and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide(MTT) value. Lipid peroxidation was evaluated using thiobarbituric acid reactive substances(TBARS) assay. Effects on antioxidant system were determined by measuring catalase, glutathione peroxidase(GSH-Px), glutathione reductase(GSH-Rd) activities as well as DNA strand breaking assay. Incubation with t-BHP alone increased GOT and LDH activities and TBARS concentration but decreased MTT reduction. Onion extracts at the concentration of 0.05 mg/ml began to decrease GOT and LDH activities induced by 1.5 mM t-BHP. Decreased MTT reduction began to be increased by onion extract at the concentration of 0.01 mg/ml. Onion extracts at the concentration of 0.01 mg/ml began to decrease TBARS concentration induced by t-BHP. Taken together, onion extracts prevented t-BHP-induced hepatocyte injury and lipid peroxidation. Catalase, GSH-Px and GSH-Rd activities of hepatocytes were significantly decreased by 1.5 mM t-BHP for 1 hr incubation. Onion extracts, on the other hand, at the concentration of 0.1 mg/ml began to prevent t-BHP-induced decrease in catalase, GSH-Px and GSH-Rd activities. Onion extracts prevented hydroxyl radical-induced single-strand breakage in dose-dependent manner when plasmid DNA was incubated with various concentrations of onion extracts in the presence of Fenton regents producing hydroxyl radical. These results demonstrate that onion extracts suppressed t-BHP-induced cytoctoxicity, decreased viability and lipid peroxidation and increased GSH-Px, GSH-Rd and catalase activities. Thus hepatoprotective and antioxidant effects of onion extract seem to be due to, at least in part, the increase in antioxidant enzyme activities as well as prevention from hydroxyl radical-induced oxidation, followed by inhibition in lipid peroxidation.
The objective of present study was to investigate the hepatoprotective and antioxidative effects of onion extracts. Primary cultures of rat hepatocytes were incubated with 1.5 mM tort-butyl hydroperoxide(t-BHP), potent oxidizing agent to liver, for 1 hr in the presence or absence of various concentrations (0, 0.01, 0.05, 0.1 or 0.3 mg/ml) of onion extract. Incubation with t-BHP increased glutamic oxaloacetic transaminase(GOT) and lactate dehydrogenase(LDH) acitivities and thiobarbituric acid reactive substances(TBARS) concentration but decreased 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide(MTT) reduction. Onion extracts at the concentration of 0.05 mg/ml decreased t-BHP-induced GOT and LDH activities. Onion extract at the concentration of 0.1 mg/ml increased t-BHP-induced MTT reduction. Onion extract at the concentration of 0.01 mg/ml decreased t-BHP-induced TBARS concentration. Taken together, onion extracts prevented t-BHP-induced hepatocyte injury and lipid peroxidation. Catalase, glutathione peroxidase(GSH-Px) and glutathione reductase(GSH-Rd) activities of hepatocytes were significantly decreased by t-BHP. Onion extracts at the concentration of 0.1 mg/ml prevented t-BHP-induced decrease in catalase, GSH-Px and GSH-Rd activities. Onion extracts prevented hydroxyl radical-induced single-strand breakage in dose-dependent manner when plasmid DNA was incubated with various concentrations of onion extracts in the presence of Fenton reagents producing hydroxyl radical. These results demonstrate that onion extracts suppressed t-BHP-induced cytoctoxicity, decreased viability and lipid peroxidation and increased GSH-Px, GSH-Rd and catalase activities. Thus hepatoprotective and antioxidant effects of onion extract seem to be due to, at least in part, the increase in antioxidant enzyme activities as well as prevention from hydroxyl radical-induced oxidation, followed by inhibition of lipid peroxidation.
In an attempt to observe the to long-term training effects, the exercise of rope-skipping was regularly loaded to nine soldiers for nine weeks. And some physical characteristics, cardiopulinonary functions. some blood constituents were measured before, during and after the load of test exercise. treadmill running, and were compared with the pre-trained values. The results obtained were as follows: 1) Body weight, body surface area, skinfold thickness and total body fat decreased sifnificantly after the training. 2) The post-trained values of MVV and $FEF_{25%}$, increased significantly. 3) By the training, heart rates decreased very significantly in the resting, exercising and recovery periods. 4) After the training, the systolic blood pressures of the resting and recovery periods decreased meaningfully, while diastolic blood pressures increased significantly through the recovery stages. 5) In spite of the training, the respiration rates never change in both the resting and the recovery periods. 6) After the training, total cholesterol concentration of the venous blood decreased significantly in the resting the early recovery phases while the blood levels of glucose and HDL-cholesterol decreased very slightly. 7) Blood lactate concentration decreased through the recovery periods and the value of the recovery 20 and 60 minutes decreased obviously, in comparison with the pre-trained values. The above results suggest that the 9 week-training of the rope-skipping brings about the decrease of the body fat contents, the enhancement of cardiopulmonary functions and some changes in the blood constituents.
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