Malondialdehyde Levels In Liver Tissues Research Articles

Short-chain chlorinated paraffins induce liver injury in mice through mitochondrial disorders and disruption of cholesterol-bile acid pathway.

Short-chain chlorinated paraffins (SCCPs) are pervasive organic pollutants recognized for their persistence and bio-toxicity. This study investigated the hepatotoxic mechanisms of SCCPs at environmentally relevant concentration (0.7 μg/kg). The results showed that SCCPs exposure in mice resulted in dysregulated blood and liver lipids, marked by elevated cholesterol levels. Additionally, liver function was compromised, as indicated by increased levels of aspartate aminotransferase, alanine aminotransferase, and alkaline phosphatase. Histopathological examination of liver tissue post-SCCPs exposure revealed hepatocyte enlargement, vacuolar degeneration, and mild ballooning degeneration. Mechanistically, SCCPs induced mitochondrial abnormalities, evidenced by heightened Hoechst 33258 fluorescence, and augmented reactive oxygen species and malondialdehyde levels in liver tissue. This was accompanied by a reduction in total antioxidant capacity, culminating in elevated apoptosis markers, including cytochrome C and caspase-3. Moreover, SCCPs perturbed hepatocellular energy metabolism, characterized by increased glycolysis, lactic acid, and fatty acid oxidation, alongside a disruption in the tricarboxylic acid cycle and a decline in mitochondrial energy metabolic function. Furthermore, SCCPs exposure downregulated the expression of genes involved in bile acid synthesis (cyp27a1, fxr, and shp), thereby precipitating the cholesterol-bile acid metabolism disorders and cholesterol accumulation. Collectively, these findings underscore that SCCPs, even at environmentally relevant levels, can induce lipid dysregulation, mitochondrial disorders and cholesterol deposition in the hepatocytes, contributing to liver damage. The study's insights contribute to a comprehension of SCCPs-induced hepatotoxicity and may inform potential preventative and treatment targets for hepatic damage associated with SCCPs exposure.

Protective effect and mechanism of quercetin on acute liver injury induced by diquat poisoning in mice

To investigate the protective effect of quercetin (QR) on acute liver injury induced by diquat (DQ) poisoning in mice and its mechanism. Eighty healthy male C57BL/6 mice with SPF grade were randomly divided into control group, DQ model group, QR treatment group, and QR control group, with 20 mice in each group. The DQ poisoning model was established by a one-time intraperitoneal injection of DQ solution (40 mg/kg); the control and QR control groups received equivalent amounts of distilled water through intraperitoneal injection. Four hours after modeling, the QR treatment group and the QR control group received 0.5 mL QR solution (50 mg/kg) through gavage. Meanwhile, an equivalent amount of distilled water was given orally to the control group and the DQ model group. The treatments above were administered once daily for seven consecutive days. Afterwards, the mice were anesthetized, blood and liver tissues were collected for following tests: changes in the structure of mice liver tissue were observed using transmission electron microscopy; the levels of serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were detected using enzyme linked immunosorbent assay (ELISA); the levels of glutathione (GSH), superoxide dismutase (SOD), and malondialdehyde (MDA) in liver tissues were measured using the water-soluble tetrazolium-1 (WST-1) method, the thiobarbituric acid (TBA) method, and enzymatic methods, respectively; the protein expressions of nuclear factor erythroid 2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1), Kelch-like ECH-associated protein 1 (Keap1), and activated caspase-9 in liver tissues were detected using Western blotting. Severe mitochondrial damage was observed in the liver tissues of mice in the DQ model group using transmission electron microscopy, yet mitochondrial damage in the QR treatment group showed significant alleviation. Compared to the control group, the DQ model group had significantly increased levels of MDA in liver tissue, serum AST, and ALT, yet had significantly decreased levels of GSH and SOD in liver tissue. In comparison to the DQ model group, the QR treatment group exhibited significant reductions in serum levels of ALT and AST, as well as MDA levels in liver tissue [ALT (U/L): 52.60±6.44 vs. 95.70±8.00, AST (U/L): 170.45±19.33 vs. 251.10±13.09, MDA (nmol/mg): 12.63±3.41 vs. 18.04±3.72], and notable increases in GSH and SOD levels in liver tissue [GSH (μmol/mg): 39.49±6.33 vs. 20.26±3.96, SOD (U/mg): 121.40±11.75 vs. 81.67±10.01], all the differences were statistically significant (all P < 0.01). Western blotting results indicated that the protein expressions of Nrf2 and HO-1 in liver tissues of the DQ model group were significantly decreased compared to the control group. On the other hand, the protein expressions of Keap1 and activated caspase-9 were conspicuously higher when compared to the control group. In comparison to the DQ model group, the QR treatment group showed a significant increase in the protein expressions of Nrf2 and HO-1 in liver tissues (Nrf2/β-actin: 1.17±0.08 vs. 0.92±0.45, HO-1/β-actin: 1.53±0.17 vs. 0.84±0.09). By contrast, there was a notable decrease in the protein expressions of Keap1 and activated caspase-9 (Keap1/β-actin: 0.48±0.06 vs. 1.22±0.09, activated caspase-9/β-actin: 1.17±0.12 vs. 1.59±0.30), the differences were statistically significant (all P < 0.01). QR may reduce acute liver injury induced by DQ poisoning in mice via activating Keap1/Nrf2 signaling pathway.

Coleus vettiveroides ethanolic root extract protects against thioacetamide-induced acute liver injury in rats.

Acute liver injury is caused by various factors, including oxidative stress and inflammation. Coleus vettiveroides, an ayurvedic medicinal plant, is known to possess antioxidant, antibacterial, and antidiabetic properties. In this current study, we investigated the protective effect of C. vettiveroides ethanolic root extract (CVERE) against thioacetamide (TAA)-induced acute liver injury in rats. A single dose of TAA (300 mg/kg, b.w., i.p.) was administered to induce acute liver injury. The treatment groups of rats were concurrently treated with CVERE (125 and 250 mg/kg, b.w., p.o.) and silymarin (100 mg/kg, b.w., p.o.), respectively. After 24 h of the experimental period, TAA-induced liver injury was confirmed by increased activity of serum transaminases and malondialdehyde levels in liver tissue, decreased levels of antioxidants, upregulated expression of the inflammatory marker gene, and altered liver morphology. Whereas CVERE simultaneous treatment inhibited hepatic injury and prevented the elevation of serum aspartate and alanine transaminases, alkaline phosphatase, and lactate dehydrogenase activities. CVERE attenuated TAA-induced oxidative stress by suppressing lipid peroxidation and restoring antioxidants such as superoxide dismutase, catalase, and reduced glutathione. Further, CVERE treatment was found to inhibit nuclear factor κB-mediated inflammatory signaling, as indicated by downregulated pro-inflammatory cytokines including tumor necrosis factor-α and interleukin-1β. Our findings suggest that CVERE prevents TAA-induced acute liver injury by targeting oxidative stress and inflammation.

Reducing effects of ginkgo biloba (egb761) extract on skeletal muscle ischemia-reperfusion injury in rats

Aim: The restoration of circulation following a period of ischemia results in the release of the metabolites that accumulate in the ischemic tissue into circulation with untoward effects on the organs. Many studies have been conducted to date into the prevention of such ischemia-reperfusion injuries. Ginkgo Biloba extract is known to have antioxidant effects, although there is a lack of data on its effects on a skeletal muscle ischemia-reperfusion model. The present study investigates the use of Ginkgo biloba extract (egb761) for the reduction of experimentally-induced skeletal muscle ischemia-reperfusion injury. Material and Methods: A total of 32 Sprague-Dawley rats were divided into four groups as follows: Group 1 (n=8), control group; Group 2 (n=8), limb ischemia model; Group 3 (n=8), ischemia-reperfusion model; and Group 4 (n=8), Ginkgo biloba group. After the models were created in each group, soleus muscle, lung and liver tissues were removed. Tissue malondialdehyde (MDA) levels were measured biochemically to demonstrate lipid peroxidation. The percentage of viable cells in the soleus muscle was calculated through a histochemical examination. Results: The comparison of soleus muscle MDA levels revealed no statistically significant difference between Group 1 and Groups 2 and 3, whereas the levels were significantly lower in Group 1 than those in Group 4 (p&lt;0.05). Similarly, there was a significant reduction in Group 4 than in Group 3 (p&lt;0.05). The analysis of lung tissue MDA levels revealed no significant difference between Group 1 and Group 2, whereas MDA levels were significantly increased in Group 3 than in Group 1 (p&lt;0.05), while there was no difference between Group 1 and Group 4. The analysis of liver tissue MDA levels showed significantly increased levels in Groups 3 and 4 than in Group 1 (p&lt;0.05). The percentage of viable cells was significantly decreased in Groups 2 and 3 than in Group 1 (p&lt;0.05). There was a significant reduction in Group 4 than in the control group. Conclusion: The results of the present study suggest that Ginkgo biloba (EGb761) extract may be used to reduce the local and systemic effects occurring after the restoration of blood flow following acute arterial occlusion. There is, however, an apparent need for large-scale, prospective, randomized trials to demonstrate the efficacy of Ginkgo biloba treatment.

Civa klorür (HgCl2) uygulanan gökkuşağı alabalığı (Oncorhynchus mykiss) karaciğer dokusunda nitrozatif ve oksidatif stresin rolü

The aim of this study was to determine oxidative stress caused by mercury chloride (HgCl2) in rainbow trout (Oncorhynchus mykiss) liver tissue. For this purpose, the LD50 value of HgCl2 on rainbow trout was determined as 551 μg/L. In the study, 40 fish in four groups were exposed to 25% and 50% (138 and 276 µg/L) of the two subletal doses of HgCl2 for 2 and 7 days, with 10 fish (n=10) in each group. To determine oxidative stress; peroxynitrite (ONOO−), total oxidant level (TOS), total antioxidant level (TAS), oxidative stress index (OSI) and malondialdehyde (MDA) were analyzed. In the study, it was observed that the differences between the groups in terms of ONOO−, TOS, TAS and OSI levels in the liver tissues was significant (P&lt;0.05), however, this difference was not significant (P&gt;0.05) in terms of MDA values. As a result, it can be concluded that HgCl2 increases ONOO−, TOS, TAS, OSI and MDA levels in liver tissue and even small doses of mercury are toxic to fish.

Effect of indomethacin on the oxidative stress of Cyprinus carpio using of biomarkers

In recent years, drugs have been identified as newly emerging and threatening the aquatic and terrestrial environments. For this purpose, in this study, the effect of indomethacin on oxidative stress in Cyprinus carpio was investigated. In order to determine the LC50, the fishes were exposed to various concentrations of indomethacin and daily losses were recorded during hours. Then the lethal toxicity (LC50) of indomethacin was obtained for carp (328.49 mg/l). In the next step, the fishes were exposed to various concentrations of indometacin in five treatments including T1 (control), T2 (0.01 mg), T3 (0.02 mg), T4 (0.05 mg), T5 (0.1 mg) for 28 days. At the end of the experiment, antioxidant enzymes such as catalase (CAT), glutathione peroxidase(GPX) and malondialdehyde(MDA) were measured in the liver and gill tissues treated fishes. The results showed that GPX enzyme activity in gill and liver tissue in all treatments increased significantly in compared to the control treatment (p<0.05). MDA levels in liver tissue in T4 and T5 groups and gill tissue in T3 and T4 groups showed a significant increase in compared to the control group (p<0.05). Also, CAT activity in liver and gill tissue in T4 and T5 groups was increased significantly in compared to the control group (p<0.05). The results of this study demonstrated that keeping indomethacin in an aqueous environment can influenc the antioxidant status and health of the fishes.

Anti-Inflammatory and Antioxidant Effect of Eucommia ulmoides Polysaccharide in Hepatic Ischemia-Reperfusion Injury by Regulating ROS and the TLR-4-NF-κB Pathway.

Eucommia ulmoides polysaccharide (EUP) has been shown to have anti-inflammatory and antioxidant effects. However, the mechanism underlying these effects has rarely been reported, and whether EUP can reduce liver injury in hepatic ischemia-reperfusion injury (HIRI) has not been reported. In this study, 40 Sprague-Dawley (SD) rats were randomly divided into 5 groups: the sham group, ischemia-reperfusion (I/R) group, and three EUP pretreatment groups (320 mg/kg, 160 mg/kg, and 80 mg/kg). SD rats were pretreated with EUP by gavage once a day prior to I/R injury for 10 days. Except for the sham group, blood flow in the middle and left liver lobes was blocked in all the other groups, resulting in 70% liver ischemia, and the ischemia and reperfusion times were 1 h and 4 h, respectively. Ischemic liver tissue and serum were obtained to detect biochemical markers and liver histopathological damage. Compared with the I/R group, after EUP pretreatment, serum alanine aminotransferase, aspartate aminotransferase, tumor necrosis factor-α, and interleukin-1β levels were significantly decreased, malondialdehyde levels in liver tissues were significantly decreased, superoxide dismutase levels were significantly increased, and the area of liver necrosis was notably reduced. To understand the specific mechanism involved, we determined the levels of Toll-like receptor- (TLR-) 4-nuclear factor-kappaB (NF-κB) pathway-associated proteins in vivo and in vitro. The data showed that EUP can reduce liver damage by decreasing ROS levels and inhibiting TLR-4-NF-κB pathway activation and may be a promising drug in liver surgery to prevent HIRI.

Short Communication: Hepatoprotective effect of methanol extract of sambiloto leaves (Andrographis paniculata) against malondialdehyde levels in liver tissues of paracetamol-induced Wistar rat

Andriani, Suseno G, Effiana, Novriany V, Fitrianingrum I. 2018. Short Communication: Hepatoprotective effect of methanol extract of sambiloto leaves (Andrographis paniculata) against malondialdehyde levels in liver tissues of paracetamol-induced Wistar rat. Nusantara Bioscience 10: 87-90. Andrographis paniculata contains andrographolide and flavonoids, which have a hepatoprotective effect. This study was aimed to examine hepatoprotective effect of Andrographis paniculata extract against liver tissues malondialdehyde (MDA) levels of paracetamol induced Wistar rat (Rattus novegicus). The study was designed with posttest-only control group conducted at Tanjungpura University, Indonesia in June 2015. A total of 30 rats at age of three weeks were divided into 6 groups. They were given toxic dose paracetamol, curcumin and A. paniculata extract in different dose. Liver tissues were tested by Wills’s method. The data was analyzed using One-way ANOVA and LSD Post-hoc test. MDA levels of liver tissues were i.e, normal control (0.34 nmol mL-1), positive control (0.34 nmol mL-1), dose 1 (0.45 nmol mL-1), dose 2 (0.55 nmol mL-1), dose 3 (0.63 nmol mL- 1 ), negative control (1.32 nmol mL-1). Result showed that MDA levels of liver tissues of negative control group were significantly different with other groups (ANOVA, p≤ 0.05). There were no significant differences between MDA levels of liver tissues of Dose 1 with normal control and positive control (ANOVA, p&gt;0.05). The methanol extract of A. paniculata has a hepatoprotective effect in (MDA) levels of paracetamol-induced Rattus novegicus with an effective dose of 500 mg kg-1.

The hepatoprotective effect of Aloe vera on ischemia-reperfusion injury in rats.

OBJECTIVE:Aloe vera is known for its antioxidant properties. In this experimental study, we aimed to investigate the efficacy of Aloe vera in ischemia-reperfusion (I/R) liver injury in rats.METHODS:Male Wistar Albino rats were divided into three groups, where the sham group (n=7) underwent no medication or surgical procedures, the I/R group (n=7) was the control group that received 45 minutes of applied abdominal aorta ischemia and rats were sacrificed 24 hours after reperfusion, and the I/R+AV group (n=7) was the treatment group that was given Aloe vera (30 mg/kg) every day followed by gastric lavage for a month before applying ischemia and performing sacrifice as in the previous group. Before sacrifice, all the liver tissues were removed. Tissues were examined for histopathological investigation, iNOS immunoreactivity and tissue biochemistry, malondialdehyde (MDA), catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px) activities.RESULTS:The SOD, CAT, and GSH-Px levels of the I/R+AV group were not significantly different from the sham group (p>0.05) but were significantly higher when compared to the I/R group. MDA levels of liver tissues were significantly lower (p<0.05) in the I/R+AV group as compared to the I/R group. Disrupted hepatic cords, sinusoidal dilatation, hemorrhage, cytoplasmic vacuolization of hepatocytes, and intensive iNOS immunoreactivity were detected in the I/R group. Decreased histopathological change score and iNOS immunoreactivity score were noticed in the I/R+AV group as compared to the I/R group.CONCLUSION:It was found that Aloe vera showed a hepatoprotective effect against I/R injury. Further research is required to determine the effective dose, administration method, and effects of Aloe vera for liver transplantation.

Hepatoprotective effect of thymol against subchronic toxicity of titanium dioxide nanoparticles: Biochemical and histological evidences

The study was aimed to investigate the protective action of thymol against nano titanium dioxide (nano-TiO2) induced hepatotoxicity in rats. To achieve this purpose, the rats were divided into four groups (n = 6) including control, nano-TiO2 (100 mg/kg), nano-TiO2 + thymol (10 mg/kg) and nano-TiO2 + thymol (30 mg/kg). Intragastric (IG) administration of nano-TiO2 for 60 consecutive days caused widespread histological changes and significantly induced oxidative stress in the liver tissues as manifested by the rise in serum transaminase activities accompanied by marked decline of enzymatic (catalase, superoxide dismutase and glutathione peroxidase) and non-enzymatic (ferric reducing antioxidant power and glutathione) antioxidant levels, and rise of malondialdehyde levels in liver tissue. Pretreatment with thymol (IG) prior to nano-TiO2 administration significantly ameliorated all of biochemical and histopathological alterations in a dose-dependent manner. In conclusion, thymol effectively protects against nano-TiO2-induced hepatotoxicity in rats by its antioxidant properties.

Ursolic Acid Improves Liver Transplantation and Inhibits Apoptosis in Miniature Pigs Using Donation After Cardiac Death

Background: Ursolic acid (UA) possesses extensive pharmacological activities, including anti-oxidation, anti-infection, anti-inflammation, anti-tumor, liver protection. This study was designed to investigate the effect of UA on liver transplantation after liver transplantation using donation after cardiac death (DCD), and to assess the mechanisms. Methods: 24 healthy experimental pigs were randomly divided into control and experimental groups. Each group received six DCD liver transplantations. In the experimental group, the recipient pigs received 120 mg/kg UA 4 h before surgery by intraperitoneal injection. The liver tissues and vein blood were collected 0 h, 1 h, 3 h, 6 h, 12 h and 24 h after transplantation. Morphological change, malondialdehyde (MDA) level, protein kinase-like ER kinase (PERK)-CHOP signaling pathway and apoptosis in liver tissue and serum aminotransferase (ALT) level were assessed. Results: Compared with control group, ALT level was significantly decreased (P<0.05) and pathological changes in liver were ameliorated in experimental group. UA treatment also decreased MDA level in liver tissue and attenuated the apoptosis. Compared with control group, Bax decreased and Bcl-2 increased in UA-treated group. Importantly, UA decreased p-PERK, PERK, p-eIF2α, eIF2α, ATF4 and CHOP levels compared with control group. Conclusion: Our results showed that UA treatment could improve the DCD liver transplantation likely through inhibiting apoptosis and PERK-CHOP pathway.

Pengaruh pemberian kecambah kacang hijau (Phaseolus radiatus (L.)) terhadap kadar malondealdehid (MDA) plasma dan jaringan hati tikus Sprague Dawley yang diberi pakan lemak tinggi

Background: High-fat diet increases the levels of fat, especially cholesterol and triglycerides that cause hyperlipidemia. Polyunsaturated fatty acids are very easily oxidized by free radicals reactive oxygens species (ROS) called lipid peroxidation, to produce compounds that malondialdehyde (MDA), is toxic and can damage plasma membrane and liver tissue. Mung bean sprouts are known to contain antioxidants which act to inhibit lipid peroxidation process.Objective: Determine the effect of mung bean sprouts to the level of plasma MDA and liver tissue of rats with high-fat diets.Method: This research is an experimental study with an only post-test design with the control group. Thirty-five male Sprague-Dawley rats were divided into 5 groups. Group K1 received fed standard; K2 received high-fat diet without mung bean sprouts. Group P1 received high-fat diet and mung bean sprouts dose of 0.5 mL/gBW. Group P2 received high-fat diet and mung bean sprouts dose of 1 mL/gBW. Group P3 received high-fat diet and vitamin E doses of 23 IU. All group were treated for 28 days. Analysis of MDA plasma and liver tissue performed after treatment.Results: Group K1 has plasma MDA levels of 1.17 ± 0.14 nmol/mL Mean MDA plasma level in the group K1 Group of K1 Mean MDA plasma level in the group K2 (39.7±0.19 nmol/mL) was higher than the group of K1 (1,17±0,14 nmol/mL), group P1 (2.94±0.09 nmol/mL), group P2 (1.73±0.08 nmol/mL) and group P3 (1.53±0.07 nmol/mL). Group K1 has liver tissue MDA Levels of 1,64±0,11 nmol/g. Mean MDA liver tissue level in the group of K2 (4.90±0.29 nmol/g) was higher than the group of P1 (3.68±0.45 nmol/g), group P2 (2.27±0.10 nmol/g), and group P3 (2.01±0.11 nmol/g).Conclusion: Level of MDA plasma and liver tissue of rat in group P1 and P2 was lower than a level of MDA plasma and liver tissue of rat in group K1, but higher than the level of MDA plasma and liver tissue of rat in group P3. There was a very strong correlation between the level of MDA plasma and liver tissue of rat was given the mung bean sprouts and high-fat diet.

Protective activity of kudzu (Pueraria thunbergiana) vine on chemically-induced hepatotoxicity: in vitro and in vivo studies.

BackgroundKudzu (Pueraria thunbergiana) root has long been used in Traditional Chinese Medicine. However, the vine of the kudzu plant has been considered waste material. This study aimed to investigate the hepatoprotective properties of the kudzu vine.MethodsWe created 0 %, 30 %, 70 %, and 95 % ethanolic kudzu vine extracts. The isoflavone contents of kudzu vine extract were quantified by high-performance liquid chromatography. Tertiary-butylhydroperoxide (t-BHP) was added to human liver-derived HepG2 cells, and the production of reactive oxygen species was measured in the presence and absence of kudzu vine extract. Antioxidant activity was evaluated in all kudzu vine extracts using a hydroxyradical scavenging assay. Thirty-five male Sprague–Dawley rats were divided into seven groups (n = 5); two groups were not given any extract or drug, one group was treated with 50 mg/kg silymarin orally for 5 days, and the remaining four groups were respectively treated with 100 mg/kg of 0 %, 30 %, 70 %, or 95 % ethanolic extract of kudzu vine orally once daily for 5 days. On day 5 the treatment groups and one untreated group were fed 0.75 ml/kg carbon tetrachloride (CCl4) to induce liver damage. Blood and liver tissue samples were collected 24 h after CCl4 administration for measurement of plasma alanine aminotransferase and aspartate aminotransferase, and concentration of malondialdehyde and glutathione in liver tissue.ResultsPuerarin was the most abundant isoflavone in kudzu vine extract. Kudzu vine extract significantly reduced the cytotoxicity and production of reactive oxygen species induced by t-BHP in a dose-dependent manner. Treatment with 0 % and 30 % ethanolic extracts of kudzu vine significantly lowered the plasma levels of alanine aminotransferase and aspartate aminotransferase in a CCl4-induced hepatotoxicity rat model (P < 0.05). Glutathione was significantly elevated in the 30 % ethanolic extract-treated group (P < 0.05), while the malondialdehyde level in liver tissue was significantly decreased in the 0 % and 30 % ethanolic extract-treated groups (P < 0.05).ConclusionsThe kudzu vine is potentially highly beneficial in treating liver damage, as it scavenges reactive free radicals and boosts the endogenous antioxidant system.

Curcumin Modulates Muscle Damage but not Oxidative Stress and Antioxidant Defense Following Eccentric Exercise in Rats.

The purpose of this study was to investigate the effects of curcumin on eccentric exercise-induced muscle damage and oxidative stress in rats. Thirty male Wistar rats were divided into four groups: Control (C; no curcumin, no exercise; n=6), Curcumin (Cur; n=8), Exercise (E; n=8) and Exercise Plus Curcumin (ECur; n=8). Curcumin was given for 20 days via oral gavage at doses of 200 mg/kg(-1) of body weight per day, dissolved in corn oil. On the 21st day eccentric exercise was provided via a treadmill run and the rats were sacrificed immediately after. Eccentric exercise resulted in significant (p<0.05) increases in all injury markers such as creatine kinase (CK) and myoglobin, but curcumin supplementation tended to decrease CK activity (p>0.05) and significantly decreased myoglobin levels (p<0.05). In blood and muscle samples, malondialdehyde (MDA) levels were not affected by either curcumin or exercise (p>0.05). MDA levels in liver tissue decreased in the ECur group, compared to the control (p<0.05). Superoxide dismutase (SOD) activities and glutathione (GSH) levels were affected by neither curcumin nor exercise (p>0.05), in blood, muscle and liver tissues. The results of this study suggest that curcumin has a protective effect on eccentric exercise induced muscle damage, and that this effect might be independent of oxidative stress and antioxidant systems.

Inhibitory Effects of Japanese Herbal Medicines Sho-saiko-to and Juzen-taiho-to on Nonalcoholic Steatohepatitis in Mice

Although Japanese herbal medicines (JHMs) are widely used in Japan, only a few studies have investigated their effects on nonalcoholic steatohepatitis (NASH). In the present study, we examined the effect of 4 kinds of JHMs [sho-saiko-to (TJ-9), inchin-ko-to (TJ-135), juzen-taiho-to (TJ-48), and keishi-bukuryo-gan (TJ-25)] on a mouse model of NASH. Db/db mice were divided into 6 groups: control diet (control), methionine- and choline-deficient diet (MCD), and MCD diet supplemented with TJ-9, TJ-135, TJ-48, and TJ-25 (TJ-9, TJ-135, TJ-48, and TJ-25, respectively). All mice were sacrificed after 4 weeks of treatment, and biochemical, pathological, and molecular analyses were performed. Serum alanine aminotransferase levels and liver histology, including necroinflammation and fibrosis, were significantly alleviated in the TJ-9 and TJ-48 groups compared with the MCD group. The expression level of transforming growth factor (TGF)-β1 mRNA in the liver was significantly suppressed by TJ-48. Although the differences were not statistically significant, the expression levels of tumor necrosis factor (TNF)-α and interleukin (IL)-6 were lower, and those of peroxisome proliferators-activated receptor (PPAR)γ were higher in the TJ-9 and/or TJ-48 groups than in the MCD group. Similarly, even though the results were not statistically significant, malondialdehyde levels in liver tissues were lower in the TJ-9 and TJ-48 groups than in the MCD group. We showed that JHMs, especially TJ-9 and TJ-48, inhibited the necroinflammation and fibrosis in the liver of a mouse model of NASH, even though the mechanisms were not fully elucidated. Further studies are needed in the future to investigate the possibility of clinical application of these medicines in the treatment for NASH.

In case of obesity, longevity-related mechanisms lead to anti-inflammation

The exact mechanisms which contribute to longevity have not been figured out yet. Our aim was to find out a common way for prompting longevity by bringing together the well-known applications such as food restriction, exercise, and probiotic supplementing in an experimental obesity model. Experimental obesity was promoted in a total of 32 young (2months old) and 32 aged (16months old) male Wistar albino rats through 8-week cafeteria diet (salami, chocolate, chips, and biscuits). Old and young animals were divided into groups each consisting of eight animals and also divided into four subgroups as obese control, obese food restriction, obese probiotic-fed and obese exercise groups. Probiotic group diet contained 0.05%w/total diet inactive and lyophilized Lactobacillus casei str. Shirota. The exercise group was subjected to treadmill running 1h/day, at 21m/min and at an uphill incline of 15% for 5days a week. Food restriction group was formed by giving 40% less food than the others. The control group was fed regular pellet feed ad libitum. This program was continued for 16weeks. Blood samples from all the groups were analyzed for fasting glucose, insulin, IGF-1, insulin-like growth factor binding protein 3 (IGFBP-3), interleukin (IL)-6, IL-12, malondialdehyde (MDA), fT3, TT3, fT4, TT4, and liver tissue MDA levels were measured. All applications showed anti-inflammatory effects through the observed changes in the levels of IGFBP-3, IL-6, and IL-12 in the young and old obese rats. While the interventions normally contribute to longevity by recruiting different action mechanisms, anti-inflammatory effect is the only mode of action for all the applications in the obesity model.

Remifentanil protects liver against ischemia/reperfusion injury through activation of anti-apoptotic pathways

BackgroundRemifentanil protects against ischemia/reperfusion (I/R)-induced organ injury, although its underlying mechanism remains elusive. This study was designed to examine the protective effect of remifentanil preconditioning, if any, against hepatic I/R injury in rats and the underlying mechanism involved. Materials and methodsAdult Sprague-Dawley rats were randomly divided into sham operation (S group), ischemia/reperfusion (I/R group), and remifentanil preconditioning (R group) groups. Rats in the I/R group were subjected to a partial (70%) hepatic ischemia for 45 min, followed by 1 h, 3 h, and 6 h of reperfusion. Rats in the R group received venous injection of remifentanil (2 μg/kg/min) from 30 min prior to hepatic ischemia to the end of ischemia. Hepatic morphology and apoptosis were examined. Markers of liver damage, oxidative stress, and inflammation were evaluated. Mitochondrial function was assessed using mitochondrial membrane potential and appearance of mitochondrial swelling. ResultsCompared with the S group, rats in the I/R group displayed a massive degenerative death in liver tissues and significantly enhanced cell apoptosis. Remifentanil preconditioning significantly reduced I/R-induced hepatocyte apoptosis. In addition, remifentanil protected against I/R-induced mitochondrial swelling and loss of membrane potential. Remifentanil preconditioning inhibited I/R-induced increases in tumor necrosis factor α, intercellular adhesion molecule 1, and nuclear factor κB p65 levels in liver tissues. Remifentanil preconditioning also inhibited the loss in superoxide dismutase and rise in malondialdehyde levels in liver tissues going through I/R injury. ConclusionsOur data revealed that remifentanil preconditioning may turn on multiple cellular pathways in hepatocytes to protect the liver from I/R injury by alleviating hepatic apoptosis.

Effect of some antioxidants on blood picture and antioxidants status in roosters exposed to oxidative stress

The present study was designed to investigate the effect of Vitamin E 600 mg/kg diet, Vitamin C 450 mg/kg diet and sodium selenite 0.5 mg/kg diet in adult white Leghorn male chickens (30 weeks), which were concomitantly exposed to oxidative stress induced by hydrogen peroxide (0.5%) supplemented with drinking water for 6 weeks on blood picture. Blood samples were collected at (0, 3, 6) weeks of treatment. Hydrogen peroxide caused a significant increase in the total leukocyte count, heterophils percentage and heterophils /lymphocytes ratio (stress index) accompanied with a significant increase in liver malondialdehyde level associated with significant decrease in hemoglobin concentration, packed cell volume, lymphocyte and esoinophil percentage. It also caused a significant decrease in liver glutathione on the 6th week of the treatment compared with control group. The antioxidants with hydrogen peroxide caused a significant decrease in the total leukocyte count, heterophils percentage and stress index accompanied with a significant decrease in malondialdehyde level in liver tissue compared with hydrogen peroxide alone and control group, beside that a significant increase in hemoglobin concentration, packed cell volume, lymphocyte, esoinophil percentage and liver glutathione level compared with hydrogen peroxide alone which returned to control group values. In general, treatments with Vitamin E, C and Sodium selenite reversed the adverse effects produced by hydrogen peroxide on certain physiological parameters in adult male chickens.

Effects of clinoptilolite treatment on oxidative stress after partial hepatectomy in rats

Clinoptilolite is a natural zeolite crystal. Cytoprotective effects of clinoptilolite have been reported. However, so far there are no data about the effects of clinoptilolite treatment on oxidative stress after partial hepatectomy. In this experimental study, the effects of clinoptilolite treatment after partial hepatectomy on oxidative stress were evaluated. There were four experimental groups (n=8): Group S, the sham group; Group H, the hepatectomy group; Group HC, the clinoptilolite treatment after partial hepatectomy group; and Group CS, the clinoptilolite-treated sham group. A 70% partial hepatectomy was performed for Group H and HC. Clinoptilolite (5mg/kg) was given to the rats orally (via gavage tube) twice a day for 10 days after hepatectomy. Malondialdehyde (MDA), Cu-Zn super oxide dismutase (SOD), and glutathione (GSH) levels were assessed to evaluate oxidative stress. Plasma and liver tissue MDA levels of Group HC were significantly lower than the H group (p=0.018 and p=0.000, respectively). Liver tissue Cu-Zn SOD activity and GSH levels of Group HC were significantly higher than Group H (p=0.003, p=0.007, respectively). Clinoptilolite administration reduces oxidant activity and supports antioxidant response after partial hepatectomy.

Hippophae rhamnoides attenuates nicotine-induced oxidative stress in rat liver

The effects of vitamin E and Hippophae rhamnoides L. (Elaeagnaceae) extract (HRe-1) on nicotine-induced oxidative stress in rat liver were investigated. Four groups, eight rats each, were used in this study, and the supplementation period was 3 weeks. The groups were: nicotine (0.5 mg/kg/day, intraperitoneal (i.p.)); nicotine plus vitamin E (75 mg/kg/day, intragastric (i.g.)); nicotine plus HRe-1 (250 mg/kg/day, i.g.); and the control group. The malondialdehyde and nitric oxide levels, glutathione peroxidase, glutathione S-transferase, glutathione reductase, superoxide dismutase, and total and non-enzymatic superoxide scavenger activities were measured spectrophotometrically in supernatants of the tissue homogenates. Nicotine increased the malondialdehyde level in liver tissue compared with control. This nicotine-induced increase in lipid peroxidation was prevented by both vitamin E and HRe-1. Superoxide dismutase activity was higher in the nicotine plus vitamin E-supplemented group compared with nicotine and control groups. Glutathione reductase activity was higher in the nicotine group compared with the control group. However, glutathione peroxidase activity in the control group was higher than the levels in the nicotine, and the nicotine plus HRe-1 supplemented groups. The nitric oxide level was higher in the nicotine group compared with all other groups. Total and non-enzymatic superoxide scavenger activities and glutathione S-transferase activity were not affected by any of the treatments. Our results suggest that Hippophae rhamnoides extract as well as vitamin E can protect the liver against nicotine-induced oxidative stress.