Curcumin decreases oxidative stress in mitochondria isolated from liver and kidneys of high-fat diet-induced obese mice

Oxidative stress plays a key role in obesity and diabetes-related mitochondrial dysfunction. Mitochondrial dysfunction is characterized by increased oxidative damage, nitric oxide (NO) synthesis, and a reduced ratio of adenosine-5'-triphosphate (ATP) production/oxygen consumption. Curcumin represents a potential antioxidant and anti-inflammatory agent. In this study, our objective was to determine the effect of curcumin treatment on oxidative stress and mitochondrial dysfunction in high-fat diet (HFD)-induced obese mice (OM). These results suggest that curcumin treatment increased oxygen consumption and significantly decreased lipid and protein oxidation levels in liver mitochondria isolated from HFD-induced OM compared with those in the untreated OM (UOM). In kidney mitochondria, curcumin treatment significantly increased oxygen consumption and decreased lipid and protein peroxidation levels in HFD-induced OM when compared with those in UOM. Curcumin treatment neither has any effect on body weight gain nor have any effects on mitochondrial NO synthesis. These findings suggest that obesity induces oxidative stress and mitochondrial dysfunction, whereas curcumin may have a protective role against obesity-induced oxidative stress and mitochondrial dysfunction.     

大蒜素对慢性铁中毒大鼠氧化应激与肝细胞自噬的抑制作用

目的探讨大蒜素(allicin)对慢性铁中毒大鼠氧化应激与肝细胞自噬的抑制作用及可能机制。方法 36只SD大鼠按体质量随机分为6组,即正常对照(饲喂基础饲料)、慢性铁中毒模型(饲喂高铁饲料)、正常+大蒜素40 mg·kg-1、慢性铁中毒+大蒜素30,40和60 mg·kg-1组,每组6只。持续饲喂6周后,取血及肝、结肠和肾组织用试剂盒测定铁含量、总铁结合力、丙二醛(MDA)含量及总超氧化物歧化酶(T-SOD)活性。透射电镜和免疫组织化学方法观察肝细胞形态结构、自噬以及胱天蛋白酶3凋亡蛋白、Ki-67细胞增殖抗原和LC3-B微管相关蛋白表达的变化。结果与正常对照组比较,模型组血清铁含量增加(P<0.01),总铁结合力下降(P<0.01),肝和结肠组织铁含量增加(P<0.05)。与模型组比较,饲喂不同剂量大蒜素大鼠血清铁含量显著下降(P<0.05),总铁结合力显著增加(P<0.05),结肠组织铁含量显著下降(P<0.05);饲喂大蒜素40和60 mg·kg-1肝组织铁含量显著下降(P<0.05)。与正常对照组比较,模型组肝和结肠组织MDA含量显著增加(P<0.05),肝组织T-SOD活性增加(P<0.01),结肠组织T-SOD活性下降(P<0.01)。与模型组比较,饲喂大蒜素组肝组织MDA含量显著下降(P<0.05),结肠和肾组织T-SOD活性显著增加(P<0.05)。与正常对照组比较,模型组肝实质细胞和肝非实质细胞Ki-67增殖抗原表达显著增加(P<0.05),胱天蛋白酶3凋亡蛋白表达无明显变化(P>0.05)。观察肝细胞超微结构,模型组大鼠肝细胞有大量铁蛋白颗粒累积,线粒体和内质网膜膨胀,胞质中形成自噬前体。模型组大鼠肝细胞LC3-B微管相关蛋白有较强表达,正常对照和正常+大蒜素组肝细胞未发现LC3-B免疫阳性染色。结论大蒜素能有效清除体内自由基,增强机体抗氧化能力,降低肝中铁诱导的氧化压力、线粒体膜的改变和细胞自噬,对慢性铁中毒肝细胞具有一定的保护作用。     

Oxidative stress induced by aluminum oxide nanomaterials after acute oral treatment in Wistar rats

This study investigated the oxidative stress induced after acute oral treatment with 500, 1000 and 2000 mg kg^?1 doses of Al₂O₃‐30 and ?40 nm and bulk Al₂O₃ in Wistar rats. Both the nanomaterials induced significant oxidative stress in a dose‐dependent manner in comparison to the bulk. There was no significant difference between the two nanomaterials. However, the effect decreased with increase with time after treatment. The histopathological examination showed lesions only in liver with Al₂O₃ nanomaterials at 2000 mg kg^?1. Copyright © 2011 John Wiley & Sons, Ltd.     

The role of oxidative stress in diazinon-induced tissues toxicity in Wistar and Norway rats

Diazinon (DZN) is an organophosphate pesticide widely used in agricultural to control insects and in veterinary medicine to control ectoparasites. This study investigated the induction of oxidative stress in the brain, heart, and spleen of Wistar and Norway rats treated with acute doses of DZN. Female Wistar and Norway rats were treated with 25, 50, 100, and 200?mg/kg of DZN by intraperitoneal injection. The animals were sacrificed 24?h after treatment, and tissues were isolated and analyzed. The result of this study shows that DZN at higher doses increased the level of malondialdehyde, superoxide dismutase and glutathione S-transferase activities and decreased glutathione (GSH) level, lactate dehydrogenase, and cholinesterase activities in the brain, heart, and spleen of both rat strains. At these concentrations, DZN toxicity also lead to a significant decrease in catalase (CAT) activity in all tissues of Wistar rat and brain of Norway rat, while it increased heart CAT activity in Norway rat. However, the alteration of these parameters was observed at lower doses of DZN in Wistar rat. These results suggest that DZN at higher doses induces the production of free radicals and oxidative stress in rat tissues and strains by alteration of antioxidant enzyme activity, depletion of GSH, and increasing lipid peroxidation. Induction of oxidative stress in DZN-treated rats is in the order of brain > heart > spleen. Wistar rats appear to be more sensitive to the effects of DZN on oxidative stress induction compared to Norway rat.     

d-α-生育酚对乙醇引发的肝脏氧化应激的影响

目的观察d-α-生育酚对乙醇诱发的小鼠肝脏氧化应激的影响并探讨其机制。方法昆明种小鼠每天给予2.4g.kg-1bw乙醇后,再给予3个不同剂量的d-α-生育酚(25、50、100mg·kg-1bw.d-1),同时设正常对照组和乙醇对照组(乙醇2.4g·kg-1bw.d-1),连续灌胃60d后,测定肝脏超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)、Na+,K+-ATP酶(Na+,K+-ATPase)、Ca2+,Mg2+-ATP酶(Ca2+,Mg2+-ATPase)、谷胱甘肽-S转移酶(GST)活力及丙二醛(MDA)的含量。结果小鼠摄入乙醇60d后,肝脏氧化应激水平明显增高。除Ca2+,Mg2+-ATPase以外,其余各项指标与正常对照组相比,差异均有显著性(P<0.05)。50mg·kg-1bw.d-1d-α-生育酚干预后,与乙醇对照组相比,GSH-Px、SOD、GST、Na+,K+-ATPase活力明显升高,MDA含量显著下降。其中,GSH-Px、Na+,K+-ATPase、MDA等3个指标在25mg·kg-1bw.d-1d-α-生育酚干预时亦出现同样的变化。结论适宜剂量的d-α-生育酚可以通过直接抑制脂质过氧化对乙醇诱发的肝脏氧化应激起保护作用。     

Sulfur mustard causes oxidative stress and depletion of antioxidants in muscles,livers, and kidneys of Wistar rats

Sulfur mustard (SM) is a chemical warfare agent with cytotoxic effect and a tight link to oxidative stress (OS). Depletion of antioxidants is considered as a cause of detrimental consequence and belongs to the important steps leading to cell death. The oxidative injury appearing after SM exposure is not well understood. Nevertheless, identification of the pathological processes would be a good opportunity to establish an efficient therapy. Here, we focused our effort on an estimation of reactive oxygen species homeostasis and apoptotic processes in Wistar rats exposed to 0–160?mg/kg of SM. We assayed antioxidant activity, thiobarbituric acid reactive substances, reduced glutathione/oxidized glutathione, metallothionein, glutathione reductase, glutathione peroxidase, glutathione S-transferase, caspase 3, and glucose in the livers, kidneys, and muscles of the animals. Significant OS, depletion of low-molecular-mass antioxidants, increase in caspase activity, and some other processes related to SM action were determined. Moreover, we infer a principal role of OS in the tested organs.     

Protective effect of lycopene on oxidative stress and antioxidant status in Cyprinus carpio during cypermethrin exposure

The aim of this study was to investigate the ameliorative properties of lycopene against the toxic effects of cypermethrin (CYP) by examining oxidative damage markers such as lipid peroxidation and the antioxidant defense system components in carp (Cyprinus carpio). The fish were divided into seven groups of 10 fish each and received the following treatments: group 1, no treatment; group 2, orally administered corn oil; group 3, oral lycopene (10 mg/kg body weight); group 4, exposure to 0.202 μg/L CYP; group 5, exposure to 0.202 μg/L CYP plus oral administration of 10 mg/kg lycopene; group 6, exposure to 0.404 μg/L CYP; and group 7, exposure to 0.404 μg/L CYP plus oral administration of 10 mg/kg lycopene. Treatment was continued for 28 days, and at the end of this period, blood and tissue (liver, kidney, and gill) samples were collected. Levels of malondialdehyde (MDA) and reduced glutathione (GSH) as well as superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH‐Px) activities were determined in blood and tissues for measurement of oxidant‐antioxidant status. MDA level, as an index of lipid peroxidation, increased in blood and tissues. Antioxidant enzyme activities in blood and tissues were modified in CYP groups compared with controls. Administration of lycopene ameliorated these parameters. The present results suggest that administration of lycopene might alleviate CYP‐induced oxidative stress. © 2011 Wiley Periodicals, Inc. Environ Toxicol 28:609–616, 2013.     

Preventive effect of Tinospora cordifolia against high-fructose diet-induced insulin resistance and oxidative stress in male Wistar rats

High intake of dietary fructose exerts a number of adverse metabolic effects. The aim of the present study was to investigate whether aqueous extract of Tinospora cordifolia stem (TCAE) alleviates high-fructose diet-induced insulin resistance and oxidative stress in rats. High-fructose diet (66% of fructose) and TCAE (400 mg/kg/day) were given simultaneously for a period of 60 days. Fructose fed rats showed hyperglycemia, hyperinsulinemia, hypertriglyceridemia, impaired glucose tolerance and impaired insulin sensitivity (P < 0.05). TCAE treatment prevented the rise in glucose levels by 21.3%, insulin by 51.5%, triglycerides by 54.12% and glucose–insulin index by 59.8% of the fructose fed rats. Regarding liver antioxidant status, fructose fed rats showed higher values of lipid peroxidation (91.3%), protein carbonyl groups (44%) and lowered GSH levels (42.1%) and, lowered activities of enzymatic antioxidants, while TCAE treatment prevented all these observed abnormalities. In conclusion, our data indicate the preventive role of T. cordifolia against fructose-induced insulin resistance and oxidative stress; hence this plant could be used as an adjuvant therapy for the prevention and/or management of chronic diseases characterized by hyperinsulinemia, hypertriglyceridemia, insulin resistance and aggravated antioxidant status.     

Nephrotoxic effects of lead nitrate exposure in diabetic and nondiabetic rats: Involvement of oxidative stress and the protective role of sodium selenite

Heavy metals are known to be toxic to organisms. The present study was undertaken to evaluate the protective effect of sodium selenite against lead nitrate (LN)‐induced nephrotoxicity in diabetic and nondiabetic rats. Animals were divided into eight groups where the first was served as a control, whereas the remaining groups were treated with sodium selenite (1 mg/kg b.w.), LN (22.5 mg/kg b.w.) and a combination of LN and sodium selenite and diabetic forms of these groups. Changes in antioxidant enzyme activities, malondialdehide levels, serum urea, uric acid, creatinine levels, body, and kidney weights and histopathological changes were determined after 28 days. LN caused severe histopathological changes, increment in urea, uric acid, creatinine, and MDA levels, also decreasing in antioxidant enzyme activities, body, and kidney weights. In sodium selenite + LN group, we observed the protective effect of sodium selenite on examining parameters. Also diabetes caused alterations on these parameters compared with nondiabetic animals. We found that sodium selenite did not show protective effect on diabetes caused damages. As a result, LN caused nephrotoxicity and sodium selenite alleviated this toxicity but sodium selenite did not protect kidneys against diabetes mediated toxicity. Also, LN caused more harmfull effects in diabetic groups compared with nondiabetic groups. © 2015 Wiley Periodicals, Inc. Environ Toxicol 31: 1229–1240, 2016.     

The effect of high-fat diet-induced obesity on cardiovascular toxicity in Wistar albino rats

The consumption of a high-fat diet (HFD) is considered a risk factor for obesity development. Nonetheless, a causal role of dietary fat has never been documented, because of inadequate animal models. In our study, one group of rats was fed with standard rat diet, while other group of rats fed with high-fat diet for 4 weeks. After 4 weeks of feeding, the hemodynamic parameters in the rats fed with HFD were significantly increased as compared with control rats. Rats fed with HFD had elevated levels of serum lipids, insulin, leptin, glucose and apolipoprotein B. Lipid peroxides and caspase-3 levels were increased while serum apolipoprotein A1 and antioxidant enzymes levels in heart tissues were decreased in HFD-induced obesity in rats as compared to normal healthy control rats fed on standard rat pellet diet. This model of diet-induced obesity will be a useful tool for studying the mechanisms by which dietary fat induces the obesity in humans.     

Mechanism of subchronic vinyl chloride exposure combined with a high-fat diet on hepatic steatosis

Vinyl chloride (VC) is a common industrial organic chlorine and environmental pollutant. In recent years, the dietary structure of residents especially Chinese has gradually shifted to western dietary patterns. VC aggravates dietary fatty acid-induced hepatic steatosis, but its mechanism is still unclear. And if the risk factors for steatosis persist, more severe diseases such as fibrosis and cirrhosis will occur. Therefore, we studied the effects and mechanisms of VC (160 and 800 mg/m³) and its metabolite (chloroacetaldehyde, 2.25, 4.5, and 9 μM) on hepatic steatosis of high-fat diet (HFD)-fed mice and palmitic acid (PA, 100 μM) treated HepG2 cells. Liver and serum biochemical indicators and pathological staining of the liver showed that the hepatic steatosis of VC combined with HFD groups was more severe than that of single-exposure groups (HFD group, low-dose VC group, and high-dose VC group). Moreover, VC enhanced HFD-induced oxidative stress (OS) and endoplasmic reticulum stress (ERS) and further upregulated the expression of sterol regulatory element-binding protein 1 (SREBP-1) and FAS. Besides, antioxidants and ERS inhibitors reduced the steatosis of HepG2 cells induced by VC metabolites and PA. These results suggest that VC exposure can enhance the degree of hepatic steatosis in HFD-fed mice. VC combined with HFD led to OS and ERS and upregulated the expression of de novo lipogenesis-related proteins, which may be related to the occurrence of hepatic steatosis. And the increased expression of CYP2E1 induced by VC combined with HFD may be the cause of OS.     

Protective effects of Phyllanthus amarus aqueous extract against renal oxidative stress in Streptozotocin -induced diabetic rats

Aim and Objectives:

In the present study, we have evaluated the antihyperglycemic, hypolipidemic and antioxidant activities of aqueous extract of Phyllanthus amarus (PAAEt) in streptozotocin (STZ)-induced diabetic rats.

Materials and Methods:

PAAEt was administered at 200 mg/kg body weight/day to normal treated (NT-group) and STZ-induced diabetic treated rats (DT-group) by gavage for eight weeks. During the experimental period, blood was collected from fasted rats at 10 days intervals and plasma glucose level was estimated. The plasma lipid profile was estimated at the end of experimental period. After the treatment, period kidney lipid peroxidation (LPO), protein oxidation and reduced glutathione (GSH) were estimated and antioxidant enzymes viz., glutathione reductase (GR), glutathione peroxidase (GPx) and glutathione-S-transferase (GST), catalase (CAT) and superoxide dismutase (SOD) were also assayed.

Results:

The significant decrease in the body weight, hyperglycemia and hyperlipidemia observed in STZ-induced diabetic rats (D-group) were rectified with PAAEt treatment in diabetic treated group (DT-group). D-group rats showed increased renal oxidative stress with increased LPO and protein oxidation. DT-group showed a significant decrease in renal LPO, protein oxidation and a significant increase in GSH content and GR, GPx and GST activities when compared with D-group. The activities of SOD and CAT decreased significantly in D-group, but were normalized in DT-group. Normal rats treated with PAAEt (NT-rats) showed a significant decrease in lipid profile, renal LPO and protein oxidation, with significant increase in renal GSH and activities of antioxidant enzymes compared to normal rats (N-group).

Conclusion:

Our results demonstrated that PAAEt with its antidiabetic, hypolipidemic and antioxidant properties could be a potential herbal medicine in treating diabetes and renal problems.     

Potassium bromate causes cell lysis and induces oxidative stress in human erythrocytes

In the present study, we have studied the effect of KBrO₃ on human erythrocytes under in vitro conditions. Erythrocytes were isolated from the blood of healthy nonsmoking volunteers and incubated with different concentrations of KBrO₃ at 37°C for 60 min. This resulted in marked hemolysis in a KBrO₃‐concentration dependent manner. Lysates were prepared from KBrO₃‐treated and control erythrocytes and assayed for various parameters. KBrO₃ treatment caused significant increase in protein oxidation, lipid peroxidation, hydrogen peroxide levels, and decrease in total sulfhydryl content, which indicates induction of oxidative stress in human erythrocytes. Methemoglobin levels and methemoglobin reductase activity were significantly increased while the total antioxidant power of lysates was greatly reduced upon KBrO₃ treatment. Intracellular production of reactive oxygen species increased in a dose dependent manner. Exposure of erythrocytes to KBrO₃ also caused decrease in the activities of catalase, glutathione peroxidase, thioredoxin reductase, glucose 6‐phosphate dehydrogenase and glutathione reductase whereas the activities of Cu‐Zn superoxide dismutase and glutathione‐S‐transferase were increased. These results show that KBrO₃ induces oxidative stress in human erythrocytes through the generation of reactive oxygen species and alters the cellular antioxidant defense system. © 2011 Wiley Periodicals, Inc. Environ Toxicol 29: 138–145, 2014.     

Di(2-ethylhexyl)phthalate-induced renal oxidative stress in rats and protective effect of selenium

This study was designed to examine the oxidative stress potential of di(2-ethylhexyl)phthalate (DEHP) on rat kidney and to evaluate possible protective effect of selenium (Se) status. Se deficiency (SeD) was produced in 3-week old Sprague?Dawley rats by feeding them ≤ 0.05 Se mg/kg diet for 5 weeks; Se supplementation group (SeS) was on 1 mg Se/kg diet. DEHP treated groups received 1000 mg/kg dose by gavage during the last 10 days of the feeding period. Activities of antioxidant selenoenzymes [glutathione peroxidase 1 (GPx1), glutathione peroxidase 4 (GPx4), thioredoxin reductase (TrxR)], catalase (CAT), superoxide dismutase (SOD), and glutathione S-transferase (GST); concentrations of total glutathione (GSH), thiols and thiobarbituric acid reactive substance (TBARS) levels were measured. DEHP treatment was found to induce oxidative stress in rat kidney, as evidenced by significant decreases in GPx1 (~20%) and SOD (~30%) activities and GSH levels (~20%), along with marked decrease in thiol content (~40%) and increase in TBARS (~30%) levels. The effects of DEHP was more pronounced in SeD rats, whereas Se supplementation was protective by providing substantial elevations of GPx1 and GPx4 activities and GSH levels. These findings emphasized the critical role of Se as an effective redox regulator and the importance of Se status in protecting renal tissue from the oxidant stressor activity of DEHP.     

Oxidative stress status in patients with acute urticaria

Background: The conflicting information related to oxidative stress status in patients with chronic idiopathic urticaria has been reported in several studies. However, the association between acute urticaria (AU) and oxidative stress has not been investigated exhaustively.

Objectives: To evaluate the role of the oxidative stress in the patients with AU by determining the oxidant/antioxidant activity in AU and to establish its clinical significance.

Methods: About 50 patients with AU, (10 males, 40 females) and 30 unrelated healthy controls (4 males, 26 females) were enrolled into the study. The activity of the antioxidant enzymes copper-zinc superoxide dismutase (Cu-Zn-SOD), glutathione peroxidase (GSH-Px) and catalase, and the levels of malondialdehyde (MDA), serum NO and protein carbonyls levels in the plasma were measured spectrophotometrically at samples.

Results: A statistically significant increase was observed in serum Cu-ZnSOD activities of the patients when compared with that of the controls (p?p?=?0.002). Serum MDA and NO levels were significantly higher in patients with AU when compared with control group (p?p?Conclusion: It seems there is an oxidative burden in the patients with AU. Cutaneous oxidative stress may play a role in pathogenesis of the disease.     

Metformin modulates cardiac endothelial dysfunction,oxidative stress and inflammation in irradiated rats: A new perspective of an antidiabetic drug

Cardiovascular disease is one of the most pivotal disorders after radiotherapy. The aim of this study investigates the possible protective effect of metformin against gamma radiation‐induced heart damage in male rats. Group 1 (control) received saline, group 2 was whole body gamma‐irradiated 5 Gy, group 3 was orally administered metformin 50 mg/kg/day for 2 weeks, group 4 received metformin 50 mg/kg/day for 1 week, then exposed to whole‐body gamma radiation at a dose of 5 Gy and continued with metformin for further 1 week. The results revealed that the administration of metformin to irradiated rats significantly ameliorated the changes in cardiac biomarkers (LDH and CK‐MB) compared with irradiated group. Heart catalase and SOD activities showed normal level when compared with the irradiated group. Also, NF‐κB, IL‐6 and TNF‐ α levels were markedly decreased compared with the corresponding values of irradiated group. Consequently, metformin reduced E‐selectin as well ICAM and VCAM‐1. These results confirmed by histopathological examination. In conclusion, concomitant administration of metformin during radiotherapy acts as a potent heart protector from oxidative stress, inflammatory mediators and endothelial dysfunction induced damages. Results thus hold a great promise for a new implication of an antidiabetic drug (metformin) as adjunct to radiotherapy.     

Transient effect of single dose exposure of Nigerian Bonny-light crude oil on testicular steroidogenesis in Wistar rats is accompanied by oxidative stress

The folkloric use of Nigerian Bonny-light crude oil (BLCO) in Niger Delta area of Nigeria is a common practice. There is increasing experimental evidence portending the adverse effects of BLCO an environmental toxicant on testicular function. We investigated the effects of single dose of BLCO (800?mg/kg body weight) on the activities of steroidogenic and antioxidant enzymes such as serum follicle stimulating hormone (FSH), luteinizing hormone (LH) and testosterone, 3 β-hydroxy-steroid dehydrogenase (3 β-HSD), 17 β-hydroxy-steroid dehydrogenase (17 β-HSD), superoxide dismutase (SOD), glutathione-S-transferase (GST) and glutathione peroxidase (GSH-Px), levels of lipid peroxidation (LPO), glutathione reduced (GSH) and steroidogenic acute regulatory (StAR) protein, in testes of rats. There was a sequential reduction in the concentration of steroid hormones and activities of steroidogenic enzymes with a concomitant decrease in levels of StAR protein, followed by a parallel increase in antioxidant enzyme activities and levels of LPO. These findings revealed inhibitory effects of BLCO on testicular steroidogenesis and the possible role of oxidative stress in testicular dysfunction observed in this study.     

Delphinidin-3-O-glucoside,an active compound of Hibiscus sabdariffa calyces,inhibits oxidative stress and inflammation in rabbits with atherosclerosis

ContextDelphinidin-3-O-glucoside (DP) is a bioactive compound of Hibiscus sabdariffa L. (Malvaceae) (Roselle) calyces and exerts endothelial protection and lipid-lowering activities, which provided a basis for the prevention and treatment of cardiovascular diseases.ObjectivesTo investigate the therapeutic effects of DP against atherosclerosis.Materials and methodsA rabbit model of atherosclerosis (AS) was established by 12 weeks of a high-fat diet (HFD). The rabbits were divided into five groups: control, AS, simvastatin (4 mg/kg), and two DP groups (10 and 20 mg/kg). After treatment with DP or simvastatin by oral gavage for 12 weeks, the lipid profiles were measured. Histopathological assessment of the aorta was performed by H&E staining. Oxidative stress and inflammation-related markers were analyzed by ELISA kit and real-time RT-PCR.ResultsDP (20 mg/kg) decreased serum TG (2.36 ± 0.66 vs. 4.33 ± 0.27 mmol/L for the AS group), TC, LDL-C, and HDL-C (all p < 0.05). DP (20 mg/kg) also reduced lipid levels in the liver and aorta. DP (20 mg/kg) down-regulated the mRNA levels of IL-6, VCAM-1, and NF-κB and up-regulated the mRNA levels of GSH-PX and SOD1.ConclusionsThis study proved that DP alleviated the HFD-induced oxidative stress and inflammation in atherosclerosis rabbits. These results provided the scientific basis for developing novel therapies.     

葛根素对链脲佐菌素诱导妊娠期糖尿病大鼠氧化应激损伤的保护作用

目的研究葛根素对链脲佐菌素诱导妊娠期糖尿病大鼠氧化应激损伤的保护作用。方法通过ip链脲佐菌素35mg/kg制备妊娠期糖尿病大鼠模型。选取64只模型大鼠并根据血糖水平随机分为模型组、葛根素40、80、160 mg/kg组,另选取16只同期妊娠的大鼠作为妊娠对照组,并取16只同龄非妊娠雌性大鼠作为非妊娠对照组。ig给药治疗,1次/d,给药容积为20 m L/kg,连续给药2周。分别于给药前和给药第7、14天测定空腹血糖水平。给药治疗2周后,测定丙氨酸转氨酶(ALT)、天门冬氨酸转氨酶(AST)、碱性磷酸酶(ALP)活性,检测血清中丙二醛(MDA)含量及总抗氧化能力(T-AOC)水平;测定肝脏组织中超氧化物歧化酶(SOD)、过氧化氢酶(CAT)活性和MDA含量。给药2周后,通过HE染色观察肝脏组织病理形态学改变。结果葛根素160 mg/kg组大鼠空腹血糖水平较模型组显著降低(P0.05、0.01)。与模型组比较,葛根素80、160 mg/kg组大鼠血清中ALT、AST活性和MDA含量均显著降低(P0.05、0.01),葛根素160 mg/kg组ALP活性显著降低(P0.01)、T-AOC水平显著升高(P0.05)。与模型组比较,葛根素80、160 mg/kg组肝脏组织中SOD活性显著升高(P0.05、0.01),MDA含量显著降低(P0.05、0.01);葛根素160 mg/kg组CAT活性显著升高(P0.01)。葛根素组大鼠肝脏组织病理形态学改变明显改善。结论葛根素对链脲佐菌素诱导妊娠期糖尿病大鼠氧化应激损伤具有保护作用,其作用机制可能与葛根素能够有效改善抗氧化酶活性、降低氧化应激损伤有关。