Effect of fermented Panax ginseng extract (GINST) on oxidative stress and antioxidant activities in major organs of aged rats

The intracellular levels of oxidant and antioxidant balances are gradually distorted during the aging process. An age associated elevation of oxidative stress occurring throughout the lifetime is hypothesized to be the major cause of aging. The present study was undertaken to evaluate the putative antioxidant activity of the fermented Panax ginseng extract (GINST) on lipid peroxidation and antioxidant status of major organs of aged rats compared to young rats. Increased levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), urea and creatinine were observed in the serum of aged rats. Increased levels of malondialdehyde (MDA) and significantly lowered activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR) and glutathione-S-transferase (GST) were observed in the liver, kidneys, heart and lungs of aged rats, when compared with those in young rats. Quantitative analysis of the non-enzymatic antioxidants such as reduced glutathione (GSH), ascorbic acid and α-tocopherol levels showed significantly lower values in the liver, kidneys, heart and lungs of aged rats. On the other hand, administration of the fermented Panax ginseng extract (GINST) to aged rats resulted in increased activities of SOD, CAT, GPx, GR and GST as well as elevation in GSH, ascorbic acid and α-tocopherol levels. Besides, the level of MDA, AST, ALT, urea and creatinine were reduced on administration of GINST to aged rats. These results suggested that treatment of GINST can improve the antioxidant status during aging, thereby minimizing the oxidative stress and occurrence of age-related disorders associated with free radicals.     

Evaluation of hepatoprotective effect of methanolic extract of Clitoria ternatea (Linn.) flower against acetaminophen-induced liver damage

Objective

To evaluate the hepatoprotective and antioxidant activity of Clitoria ternatea (C. ternatea) flower extract against acetaminophen-induced liver toxicity.

Methods

The antioxidant property of C. ternatea flower extract was investigated by employing established in vitro antioxidant assay. The C. ternatea flower extract was studied in this work for its hepatoprotective effect against acetaminophen-induced liver toxicity in mice. Activity was measured by monitoring the levels of aspartate aminotransferase, alanine aminotransferase, billirubin and glutathione with histopathological analysis.

Results

The amount of total phenolics and flavonoids were estimated to be 105.40±2.47 mg/g gallic acid equivalent and 72.21±0.05 mg/g catechin equivalent respectively. The antioxidant activity of C. ternatea flower extract was 68.9% at a concentration of 1 mg/mL and was also concentration dependant, with an IC₅₀ value of 327.00 µg/mL. The results of acetaminophen-induced liver toxicity experiment showed that mice treated with the extract (200 mg/kg) showed a significant decrease in alanine aminotransferase, aspartate aminotransferase, and bilirubin levels, which were all elevated in the paracetamol group (P<0.05). Meanwhile, the level of glutathione was found to be restored in extract treated animals compared to the groups treated with acetaminophen alone (P<0.05). Therapy of extract also showed its protective effect on histopathological alterations and supported the biochemical finding.

Conclusion

The present work confirmed the hepatoprotective effect of C. ternatea flower against model hepatotoxicant acetaminophen.     

Influence of exercise training frequency on cardiac and hepatic oxidative stress in rats

The present study investigated the influence of different frequencies of moderate exercise (13 weeks of treadmill running at 60% of maximal oxygen consumption) on oxidative stress in the heart and liver in rats. Oxidative stress was evaluated by chemiluminescence and lipid peroxidation (LPO) through thiobarbituric acid reactive substances. Activities of superoxide dismutase (SOD), glutathione peroxidase (GHPx) and catalase (CAT) were also measured. The animals were divided into four groups: control (C), acute ([A], only one exercise session at the end of 13 weeks), low frequency ([LF], one session a week for 13 weeks) and high frequency ([HF], five sessions a week for 13 weeks). Chronic exercise promoted cardiac hypertrophy in the HF group. Myocardial LPO in groups A and LF was increased, whereas in the HF group, it was decreased when compared with group C. The HF group demonstrated decreased myocardial SOD and GHPx activities and increased CAT activity. All exercise groups exhibited an increase in LPO in the liver compared with group C. SOD activity in liver was lower in the HF group and higher in the LF group as compared with group C. GHPx activity was higher in group A in relation to group C. Hepatic CAT activity was higher in groups A, LF and HF. It is suggested that chronic exercise training at a submaximal level is better than infrequent exercise bursts to promote metabolic adaptations that minimize oxidative stress.     

Hepatoprotective and antioxidant activity of pentagamavunon-0 against carbon tetrachloride-induced hepatic injury in rats

ObjectiveTo investigate the hepatoprotective and antioxidant activity of pentagamavunon-0(PGV-0) against CCl₄-induced hepatic injury in rats.MethodsThe groups of animals were administered with PGV-0 at the doses 2.5, 5, 10, and 20 mg/kgb.w., p.o. once in a day for 6 days and at day 7 the animals were administrated with carbon tetrachloride (CCl) (20%, 2 mL/kgb.w. in liquid paraffin (i.p.). The effect of PGV-0 on serum transaminase (SGPT), alkaline phosphates (ALP) and total bilirubin were determined in CCl₄-induced hepatotoxicity in rats. Further, the effects of PGV-0 on glutathione (GSH) content, catalase (CAT) and NO free radical scavenging activity also were investigated.ResultsThe results demonstrated that PGV-0 significantly reduced the activity of SGPT, serum ALP and total bilirubin in CCl₄induced rat hepatotoxicity. PGV-0 has effect on the antioxidant and free radical defense system. It prevented the depletion level of GSH and decrease activity of CAT in CCl₄-induced liver injury in rats. PGV-0 also demonstrated the free radical scavenger effects on NO free radical scavenging activity with ES value of 32.32μM.ConculsionAll of our findings suggests that PGV-0 could protect the liver cells from CCl₄-induced liver damages and the mechanism may through the antioxidative effect of PGV-0 to prevent the accumulation of free radicals and protect the liver damage.     

Effect of haemodialysis on the oxidative stress and antioxidants in diabetes mellitus

Abstract Oxidative stress has been defined as a loss of counterbalance between free radical or reactive oxygen species (ROS) production and antioxidant systems. It is involved in the pathogenesis of different chronic diseases. High levels of ROS production via different biochemical mechanisms accompany diseases like type 2 diabetes mellitus (DM) and end-stage renal disease (ESRD). Elevated oxidative status and reduced antioxidant defence systems in patients with DM and ESRD accelerate the prevalence of atherosclerosis and other chronic complications. Our aim was to reveal the effects of diabetes and haemodialysis (HD) separately and together on oxidative stress. In our study, we included 20 diabetic (DM) patients with no renal disease, 20 non-diabetic haemodialysis (HD), 20 diabetic haemodialysis (DHD) patients and 20 healthy volunteers. We have determined the levels of lipid peroxidation expressed as thiobarbituric acid-reactive substances (TBARS), oxidative protein damage as indicated by protein carbonyl (PCO) content and activities of antioxidant enzymes including superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSHPx) in all patient groups and healthy subjects. We found enhanced oxidative stress in all patient groups due to an increase in lipid peroxidation (TBARS) and increased oxidative protein damage in terms of PCO content and reduced activities of SOD, CAT and GSH-Px. Oxidative stress was more profound in diabetic patients undergoing haemodialysis. We conclude that both diabetes and dialysis increase oxidative stress and their combined effect on oxidative stress is the highest in magnitude as observed in diabetic patients undergoing haemodialysis.     

A dual effect of N-acetylcysteine on acute ethanol-induced liver damage in mice.

Reactive oxygen species (ROS) have been associated with acute ethanol-induced liver damage. N-acetylcysteine (NAC) is a glutathione (GSH) precursor and direct antioxidant. In this study, we investigated the effects of NAC on acute ethanol-induced liver damage. Female ICR mice were administered by gavage with a single dose of ethanol (6g/kg). NAC was administered in two different modes. In mode A, mice were injected with different doses of NAC at 30min before ethanol. In mode B, mice were injected with different doses of NAC at 4h after ethanol. Acute ethanol-induced liver damage was estimated by measuring serum alanine aminotransferase (ALT) activity and histopathological changes. Result showed that a single dose of ethanol (6g/kg) caused a significant increase in serum ALT activity, followed by microvesicular steatosis and necrosis in mouse liver. Pretreatment with NAC significantly protected against acute ethanol-induced liver damage in a dose-independent manner. Correspondingly, pretreatment with NAC significantly attenuated acute ethanol-induced lipid peroxidation and GSH depletion and inhibited hepatic TNF-alpha mRNA expression. By contrast, post-treatment with NAC aggravated ethanol-induced hepatic lipid peroxidation and worsened acute ethanol-induced liver damage in a dose-dependent manner. Taken together, NAC has a dual effect on acute ethanol-induced liver damage. Pretreatment with NAC prevent from acute ethanol-induced liver damage via counteracting ethanol-induced oxidative stress. When administered after ethanol, NAC might behave as a pro-oxidant and aggravate acute ethanol-induced liver damage.     

Protective effect of Ferula gummosa hydroalcoholic extract against nitric oxide deficiency-induced oxidative stress and inflammation in rats renal tissues

Abstract

Nitric oxide (NO) synthase inhibition increases hypertension and causes renal injury. Ferula gummosa is used in Iranian traditional medicine for treatment of several diseases and has been reported to exert a potent anti-inflammatory and antioxidant action. The aim of this investigation was to evaluate the renoprotective effects of hydroalcoholic extract of Ferula gummosa (HEG) on Nω-nitro-l-arginine methyl ester (l-NAME)-induced oxidative stress and inflammation and explore the mechanisms that link NO deficiency with altered renal heat shock protein (HSP70). Rats were injected intraperitoneally with l-NAME (10?mg/kg) to induce renal injury. Simultaneously, HEG (90?mg/kg) was administered by gastric gavage to l-NAME-treated rats for 6 days/week during an 8-week period. Renal thiobarbituric acid reactive substances (TBARS), superoxide dismutase (SOD), interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-α), HSP70, plasma NO and total antioxidant capacity (TAC) were evaluated. The administration of l-NAME significantly increased renal TBARS, TNF-α, IL-6, HSP70 levels and decreased renal SOD activity, that these changes were accompanied by the reduced plasma NO and TAC levels. HEG administration decreased TBARS, HSP70, TNF-α and IL-6 levels and increased SOD activity in the kidney tissues of l-NAME treated rats (p?<?0.05). Also, plasma TAC level and NO bioavailability have been elevated after administration of HEG (p?<?0.05). These findings support that NO deficiency induces renal stress oxidative and inflammation, which markedly increased renal HSP70 and HEG could protect kidney against these damaging effects via its anti-oxidative, anti-inflammatory action and modulate renal HSP70.     

Protective effect of Sida cordata leaf extract against CCl4 induced acute liver toxicity in rats

ObjectiveTo investigate the hepatoprotective potential of Sida cordata (Malvaceae) (S. cordata) in experimental rats to validate its traditional claim.MethodsWister albino rats were divided into 6 groups: Group I served as control; Group II served as hepatotoxic (CCl₄ treated) group; Group III, IV and V served as (100, 200 and 400 mg/kg b.w.) S. cordata leaf extract (SCLE) treated groups; Group VI served as positive control (Silymarin) treated group. Liver marker enzymes serum glutamate oxyloacetic transaminase, serum glutamic pyruvic transaminase, pancreatic enzymatic antioxidants superoxide dismutase (SOD), lipid peroxidation, catalase (CAT), reduced glutathione (GSH) were measured and compared along with histopathological studies.ResultsObtained results show that the treatment with SCLE significantly (P<0.05-<0.001) and dose-dependently reduced CCl₄ induced elevated serum level of hepatic enzymes. Furthermore, SCLE significantly (up to P<0.001) reduced the lipid peroxidation in the liver tissue and restored activities of defence antioxidant enzymes GSH, SOD and CAT towards normal levels, which was confirmed by the histopathological studies.ConclusionsThe results of this study strongly indicate the protective effect of SCLE against CCl₄ induced acute liver toxicity in rats and thereby scientifically support its traditional use.     

The effect of celecoxib, a selective COX-2 inhibitor, on liver ischemia/reperfusion-induced oxidative stress in rats.

This study examined the effects of celecoxib on hepatic ischemia/reperfusion (I/R) injury in rats. A total of 40 male Sprague-Dawley rats weighing 190-210g were randomized into 4 groups of 10: (1) controls: data from unmanipulated animals; (2) sham group: rats subjected to the surgical procedure, except for liver I/R, and given saline; (3) I/R group: rats that underwent liver ischemia for 1h followed by reperfusion for 45min; (4) I-R/Celecoxib group: rats pretreated with celecoxib (3mgkg(-1), i.p.) 40min before liver I/R. Tc-99m sulfur colloid images were used to measure the uptake ratio and perfusion index. Liver tissues were taken to determine SOD, CAT, GSH-Px, and MDA levels and for biochemical and histological evaluation. The plasma ALT, AST, GGT, and LDH activities were higher in group 3 than in group 4. The uptake ratio was significantly lower in group 3 compared to groups 1, 2, and 4. In addition, in group 4, the uptake ratio and perfusion index were also significantly higher compared to group 3. MDA values and the hepatic injury score decreased, while the SOD, CAT, and GSH-Px values increased in group 4 compared to group 3. In group 3, hepatocytes were swollen with marked vacuolization. Group 4 showed well preserved liver parenchyma with hepatocytes arranged radially around the central vein; there were regular sinusoidal structures with normal morphology without any signs of congestion. We showed that celecoxib has beneficial effects in hepatic I/R injury and may protect the liver.     

Lead exposure increases oxidative stress in the gastric mucosa of HCI/ethanol-exposed rats

AIM: To investigate the role of reactive oxygen species in the ulcer-aggravating effect of lead in albino rats.METHODS: Albino Wistar rats were randomly divided into three groups and treated orally with 100 mg/L (low dose) or 5000 mg/L (high dose) of lead acetate for 15 wk. A third group received saline and served as control.At the end of wk 15, colorimetric assays were applied to determine the concentrations of total protein and nitrite, the activities of the oxidative enzymes catalase and superoxide dismutase, and lipid peroxidation in homogenized gastric mucosal samples.RESULTS: Exposure of rats to lead significantly increased the gastric mucosal damage caused by acidified ethanol. Although the basal gastric acid secretory rate was not significantly altered, the maximal response of the stomach to histamine was significantly higher in the lead-exposed animals than in the unexposed control group. Exposure to low and high levels of lead significantly increased gastric lipid peroxidation to 183.2% ± 12.7% and 226.1% ± 6.8% of control values respectively (P ＜ 0.0). On the other hand, lead exposure significantly decreased catalase and superoxide dismutase (SOD) activities and the amount of nitrite in gastric mucosal samples.CONCLUSION: Lead increases the formation of gastric ulcers by interfering with the oxidative metabolism in the stomach.     

Laboratory evaluation of aqueous leaf extract of Tephrosia vogelii against larvae of Aedes albopictus (Diptera: Culicidae) and non-target aquatic organisms

Mosquito control using insecticides has been the most successful intervention known to reduce malaria prevalence or incidence. However, vector control is facing a threat due to the emergence of resistance to synthetic insecticides. Insecticides of botanical origin may serve as suitable alternative biocontrol techniques in the future. In this research, the leaf aqueous leachate of Tephrosia vogelii was evaluated for its toxicity against larvae of the most invasive mosquito worldwide, Aedes albopictus (Diptera: Culicidae), and toward adults of the water flea, Daphnia magna (Cladocera: Crustacea) and Oreochromis niloticus, two non-target aquatic organisms that share the same ecological niche of A. albopictus. The leaf aqueous leachate of T. vogelii was evaluated against fourth-instar larvae, non-blood fed 3–5 days old laboratory strains of A. albopictus under laboratory condition. In addition, the objective of the present work was to study the environmental safety evaluation for aquatic ecosystem. Mortality was then recorded after 7 d exposure. The leaf aqueous leachate of T. vogelii showed high mosquitocidal activity against larvae of A. albopictus, with a LC₅₀ = 1.18 μg/mL. However, it had a remarkable acute toxicity also toward adults of the non-target arthropod D. magna, with a LC₅₀ = 0.47 μg/L and O. niloticus with a LC₅₀ = 5.31 μg/L. The present findings have important implications in the practical control of mosquito larvae in the aquatic ecosystem, as the medicinal plants studied are commonly available in large quantities. The extract could be used in stagnant water bodies for the control of mosquitoes acting as vector for many communicable diseases.     

Lead exposure increases oxidative stress in the gastric mucosa of HCl/ethanol-exposed rats

AIM To investigate the role of reactive oxygen species in the ulcer-aggravating effect of lead in albino rats.METHODS Albino Wistar rats were randomly divided into three groups and treated orally with 100 mg/L (low dose) or 5000 mg/L (high dose) of lead acetate for 15 wk. A third group received saline and served as control.At the end of wk 15, colorimetric assays were applied to determine the concentrations of total protein and nitrite, the activities of the oxidative enzymes catalase and superoxide dismutase, and lipid peroxidation in homogenized gastric mucosal samples.RESULTS Exposure of rats to lead significantly increased the gastric mucosal damage caused by acidified ethanol. Although the basal gastric acid secretory rate was not significantly altered, the maximal response of the stomach to histamine was significantly higher in the lead-exposed animals than in the unexposed control group. Exposure to low and high levels of lead significantly increased gastric lipid peroxidation to 183.2% ± 12.7% and 226.1% ± 6.8% of control values respectively (P ＜ 0.0). On the other hand, lead exposure significantly decreased catalase and superoxide dismutase (SOD) activities and the amount of nitrite in gastric mucosal samples.CONCLUSION Lead increases the formation of gastric ulcers by interfering with the oxidative metabolism in the stomach.     

Cordycepin (3′-deoxyadenosine) attenuates age-related oxidative stress and ameliorates antioxidant capacity in rats

Free radical-induced oxidative damage is considered to be the most important consequence of the aging process. The activities and capacities of antioxidant systems of cells decline with increased age, leading to the gradual loss of pro-oxidant/antioxidant balance and resulting in increased oxidative stress. Our investigation was focused on the effects of cordycepin (3′-deoxyadenosine) on lipid peroxidation and antioxidation in aged rats. Age-associated decline in the activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR), glutathione-S-transferase (GST), reduced glutathione (GSH), vitamin C and vitamin E, and elevated levels of malondialdehyde (MDA) were observed in the liver, kidneys, heart and lungs of aged rats, when compared to young rats. Furthermore, serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), urea, and creatinine were found to be significantly elevated in aged rats compared to young rats. Aged rats receiving cordycepin treatment show increased activity of SOD, CAT, GPx, GR and GST, and elevated levels of GSH, and vitamins C and E such that the values of most of these parameters did not differ significantly from those found in young rats. In addition, the levels of MDA, AST, ALT, urea and creatinine became reduced upon administration of cordycepin to aged rats. These results suggest that cordycepin is effective for restoring antioxidant status and decreasing lipid peroxidation in aged rats.     

Effects of acute and chronic administration of methylprednisolone on oxidative stress in rat lungs

Objective:

To determine the effects of acute and chronic administration of methylprednisolone on oxidative stress, as quantified by measuring lipid peroxidation (LPO) and total reactive antioxidant potential (TRAP), in rat lungs.

Methods:

Forty Wistar rats were divided into four groups: acute treatment, comprising rats receiving a single injection of methylprednisolone (50 mg/kg i.p.); acute control, comprising rats i.p. injected with saline; chronic treatment, comprising rats receiving methylprednisolone in drinking water (6 mg/kg per day for 30 days); and chronic control, comprising rats receiving normal drinking water.

Results:

The levels of TRAP were significantly higher in the acute treatment group rats than in the acute control rats, suggesting an improvement in the pulmonary defenses of the former. The levels of lung LPO were significantly higher in the chronic treatment group rats than in the chronic control rats, indicating oxidative damage in the lung tissue of the former.

Conclusions:

Our results suggest that the acute use of corticosteroids is beneficial to lung tissue, whereas their chronic use is not. The chronic use of methylprednisolone appears to increase lung LPO levels.     

Hepatoprotective effect of Cichorium intybus L.,a traditional Uighur medicine,against carbon tetrachloride-induced hepatic fibrosis in rats

AIM:To investigate the hepatoprotective effect of a Cichorium intybus L.extract(CIE)on CCl4-induced hepatic fibrosis in rats.METHODS:Seventy-two male Wistar albino rats were randomly divided into six groups of twelve rats each.The normal control group was allowed free access to food and water.Liver injury was performed in the remaining five groups with an i.p.injection of a 1.0mL/kg CCl4 and olive oil(2:3 v/v)mixture,twice weekly for 8 weeks.All rats,with the exception of the injury model group,were intragastrically(i.g.,)administered quantum satis(q.s.)dosages[CIE group:6,18,and 54 mg/kg,respectively;Fu Fang Bie Jia Ruan Gan Pian(FFBJRGP)group:780 mg/kg].The oral administration of different drugs was performed on the day before CCl4 administration and subsequently once per day for8 wk.The serum levels of aspartate aminotransferase(AST),alanine aminotransferase(ALT),hexadecenoic acid(HA),laminin(LN),hydroxyproline(Hyp),and glutathione(GSH),malondialdehyde(MDA)and superoxide dismutase(SOD)in the rat livers were measured.Histopathological changes in the liver were assessed for each group using HE staining and a Masson Trichrome examination.The expression of transforming growth factor-β1(TGF-β1)andα-smooth muscle actin(α-SMA)was examined by immunohistochemical analysis.RESULTS:CIE at oral doses of 6,18,and 54 g/kg per day showed a significant hepatoprotective effect,especially at a dose of 54 g/kg per day.CIE doses reduced the levels of AST(149.04±34.44,P<0.01),ALT(100.72±27.19,P<0.01),HA(548.50±65.09,P<0.01),LN(28.69±3.32,P<0.01)and Hyp(263.33±75.82,P<0.01).With regards to hepatoprotective activity,the CIE dose of 54 g/kg per day produced the largest significant effect by increasing GSH(3.11±0.81),SOD(269.98±33.77,P<0.01)and reducing MDA(2.76±0.51,P<0.01)levels in the liver.The expressions of TGF-β1 andα-SMA were measured by immunohistology and found to be significantly reduced by CIE in a dose-dependent manner.     

Hepatoprotective effect of manual acupuncture at acupoint GB34 against CCl4-induced chronic liver damage in rats

AIM: To investigate the hepatoprotective effect of manual acupuncture at Yanglingquan (GB34) on CCl4-induced chronic liver damage in rats. METHODS: Rats were injected intraperitoneally with CC4l (1 mL/kg) and treated with manual acupuncture using reinforcing manipulation techniques at left GB34 (Yanglingquan) 3 times a week for 10 wk. A non-acupoint in left gluteal area was selected as a sham point. To estimate the hepatoprotective effect of manual acupuncture at GB34, measurement of liver index, biochemical assays including serum ALT, AST, ALP and total cholesterol, histological analysis and blood cell counts were conducted. RESULTS: Manual acupuncture at GB34 reduced the liver index, serum ALT, AST, ALP and total cholesterol levels as compared with the control group and the sham acupuncture group. It also increased and normalized the populations of WBC and lymphocytes. CONCLUSION: Manual acupuncture with reinforcing manipulation techniques at left GB34 reduces liver toxicity, protects liver function and liver tissue, and normalizes immune activity in CCl4-intoxicated rats.