��-Glucosidase inhibitory and antioxidant properties and antidiabetic activity of Hypericum ascyron L.

Different solvent extracts of Hypericum ascyron L. were evaluated by α-glucosidase inhibitory activity and DPPH, ABTS and FRAP assays, respectively, for antioxidant properties in vitro. EtOAC and MeOH extracts showed stronger inhibiting activity against α-glucosidase and rat intestinal α-glucosidase compared with acarbose as positive control. Eight known compounds were isolated from EtOAC and MeOH extracts and screened for α-glucosidase inhibitory and antioxidant activities. Kaempferol and ursolic acid were active compounds of α-glucosidase inhibitory effect in EtOAC extract. Quercetin-3-O-β-d-galactoside, quercetin-3-O-β-d-glucoside and kaempferol from EtOAC and MeOH extracts showed moderate or lightly low antioxidant activity with BHT as positive control. The antidiabetic activity of EtOAC and MeOH extracts was determined in vivo. After intragastric administration of EtOAC extract (500 mg/kg body weight per day) and MeOH extract (500 mg/kg) to groups of on alloxan-induced diabetic mice for 8 days, the level of blood glucose in serum significantly decreased (P < 0.01 and P < 0.05, respectively), the blood lipid level of TC and TG lowered, and the oxidant stress and oxidative damage to tissues were inhibited by decreasing the level of MDA (P < 0.01 and P < 0.01, respectively) and lightly increasing the level of SOD. The result showed that H. ascyron may be a good sources of natural antioxidants and α-glucosidase inhibitor using for the therapy of hyperglycemic and its complication.     

Effects of the hydroalcoholic extract of <Emphasis Type="Italic">Phyllanthus niruri</Emphasis> and its isolated compounds on cyclophosphamide-induced hemorrhagic cystitis in mouse

The effects of Phyllanthus niruri hydroalcoholic extract and the isolated compounds quercetin, rutin, and gallic acid were examined in the mouse model of cyclophosphamide (CYP)-induced hemorrhagic cystitis (HC). HC was induced by a single CYP injection (300 mg/kg, IP), and the animals were evaluated 4 and 6 h after. Some animals were orally treated with the reference compound 2-mercaptoethane sodium sulfonate (Mesna) 80 mg/kg (30 min before CYP) and 160 mg/kg (2 h after CYP). Other groups were treated with P. niruri extract (30 and 50 mg/kg), or quercetin, rutin, and gallic acid (10 and 20 mg/kg), given orally, at the same intervals described for Mesna. P. niruri extract and its active components produced a significant attenuation of the nociception, edema, and hemorrhage evoked by CYP, which was similar to that seen for Mesna. Gallic acid and rutin displayed greater anti-inflammatory effects, whereas quercetin presented superior antinociceptive activities. Noteworthy is that P. niruri extract and compounds significantly reduced CYP-induced liver lipid peroxidation. Our results shed new light on the beneficial effects of P. niruri extract and its active compounds in attenuating the collateral effects elicited by the chemotherapeutic agent CYP.     

江苏地产白首乌 C21甾体苷对高血脂大鼠的肝脏保护作用和抗氧化作用研究

目的：研究江苏地产白首乌 C21甾体苷对实验性高脂血症大鼠的肝脏功能和脂质过氧化的影响。方法建立实验性高脂血症大鼠模型,对造模成功的高脂血症大鼠分别给予白首乌 C21甾体（20 mg/ kg,40 mg/ kg）、阿托伐他汀钙10 mg/ kg 和1％羧甲基纤维素钠溶液灌胃,1次/ d,连续给药2周,同时设正常对照组。比较体重变化,计算肝脏系数;检测血清和肝脏中丙氨酸氨基转移酶（ALT）、天冬氨酸氨基转移酶（AST）;行肝脏病理学检查。并行血清中超氧化物歧化酶（SOD）、丙二醛（MDA）和谷胱甘肽过氧化物酶（GSH-Px）的检测。结果白首乌 C21甾体苷给药2周,能够有效控制高脂血症模型大鼠肝脏系数,病理学切片显示能改善肝脏脂肪变性。白首乌高剂量组能降低高血脂大鼠的 SOD 和 GSH-Px 水平,各用药组均能显著降低高血脂大鼠升高的 MDA 含量（ P ＜0.05）。结论白首乌 C21甾体苷具有良好改善高脂血症大鼠肝脏功能的作用,能对抗高血脂大鼠脂质过氧化。     

Effects of Rutin on Lipid Profile in Hypercholesterolaemic Rats

Abstract: Rutin (3, 3′, 4′, 5, 7‐pentahydrohyflavone‐3‐rhamnoglucoside) is a flavonoid of the flavonol type. Rutin is found in many plants and is also an important dietary constituent of food and plant‐based beverages. Rutin has several pharmacological properties including antioxidant and cardioprotective activities. Also, it was identified that rutin is the major low‐density lipoprotein (LDL) antioxidant compound of mulberry in an in vitro study. The effects of rutin were tested by using it as a supplement in a high‐cholesterol diet. Male rats were fed a high‐cholesterol diet (1 ml/100 g) for 4 weeks with rutin (10 or 100 mg/kg) or rutin 100 mg/kg and lovastatin supplementation to study the hypocholesterolaemic effects of rutin on plasma lipid levels, hepatic enzyme activity, and liver tissue. Feeding the animals a high‐cholesterol diet resulted in marked hypercholesterolaemia and increased the serum level of LDL cholesterol (LDL‐C). Rutin (at 100 mg/kg) alone or in combination with lovastatin significantly reduced the levels of total cholesterol, and LDL‐C and also markedly decreased liver enzymes and weight in animals with a high‐cholesterol diet. Our findings show that 100 mg/kg of rutin alone or with lovastatin supplementation lowered liver weight and enzymes as well as plasma total cholesterol and LDL. The hepatic histopathological results reflect the correlation of rutin and lovastatin combination with both liver weight and the levels of plasma total cholesterol and LDL‐C. These results indicate that rutin in combination with lovastatin has increased anti‐hypercholesterolaemic effects in an animal model.     

Possible involvement of nitric oxide mechanism in the neuroprotective effect of rutin against immobilization stress induced anxiety like behaviour,oxidative damage in mice

Dietary supplements are widely used to manage stress and related consequences. However, the exact pathological mechanism and cellular cascades involved in the action of these supplements are not properly understood so far. Therefore, the present study has been designed to explore the neuroprotective mechanism of rutin against immobilization stress-induced anxiety-like behavioural and oxidative damage in mice. Laboratory Animal Centre A-strain (laca) mice were used in the present study. Rutin (20, 40, and 80 mg/kg), l-arginine (100 mg/kg), l-nitroarginine methyl ester (l-NAME) (5 mg/kg) and vitamin-E (50 mg/kg) were administered for 5 days before 6 h immobilization stress on 6th day. Various behavioural parameters (mirror chamber test, locomotor activity) followed by biochemical parameters (lipid peroxidation, nitrite concentration, reduced glutathione and catalase) in brain and then serum corticosterone level were assessed. 6 h immobilization stress produced anxiety-like behavioural in mirror chamber test, raised corticosterone level and oxidative stress (as evidenced by rise in lipid peroxidation, nitrite concentration, depletion of reduced glutathione and catalase activity) significantly as compared to naive group. 5 days pre-treatment with rutin (40 and 80 mg/kg) causes a significant attenuation of locomotor activity, corticosterone level, oxidative stress as compared to control. Further, l-arginine (100 mg/kg) pre-treatment significantly reversed the protective effect of rutin (40 mg/kg) in 6 h immobilized animals. However, l-NAME (5 mg/kg) pre-treatment with rutin (40 mg/kg) potentiated their protective effect which was significant as compared to their effect per se. The present study suggests the involvement of nitric oxide mechanism in the neuroprotective effect of rutin against immobilization stress-induced anxiety-like behaviour and oxidative damage in mice.     

Hypolipidemic and antioxidant effects of ethanol extract of Cassia fistula fruit in hyperlipidemic mice

Context: The plant Cassia fistula L. (Caesalpiniaceae) fruit was widely used by traditional practitioners to treat cardiovascular diseases (CVDs) in India. Hyperlipidemia is a lipid metabolism disorder and the major risk factor for the development of CVDs. Although most of the current hypolipidemic drugs are expensive and have potential side effects, the research focusing on natural alternative medicines is relevant.

Objective: To investigate the hypolipidemic and antioxidant effects of ethanol extract of C. fistula fruit (CFE) in high-fat diet (HFD) induced hyperlipidemia in mice.

Materials and methods: Oral administration of CFE at 100, 300 and 500?mg/kg body weight on HFD induced hyperlipidemia mice for 30 days. The standard drug atorvastatin (20?mg/kg) was used to compare the efficacy of CFE. Hypolipidemic effect was evidenced by the measurement of serum lipid profile and further confirmed by Oil Red O staining of adipose tissue. The hepatic and cardiac melondialdehyde (MDA) level and antioxidant enzyme activities including superoxide dismutase, catalase and glutathione peroxidase were determined.

Results: Treatment with CFE at different doses has significantly restored the levels of serum lipid, MDA and enzymes activities in the liver and heart of hyperlipidemia mice. Oil Red O staining of visceral adipose tissue has shown marked reduction of lipid accumulation in adipocytes; whereas, administration of CFE at 500?mg/kg showed remarkable (p?<?0.001) hypolipidemic and antioxidant effects in HFD fed mice.

Conclusion: C. fistula fruit demonstrated hypolipidemic and antioxidant properties in vivo and the results corroborate the use of this plant in traditional medicine for cardiac ailments.     

青葙总皂苷对高血脂动物脂质代谢的影响

目的 探讨青葙总皂苷（CES）对高血脂动物脂质代谢的影响。方法 建立金黄地鼠、家兔高血脂模型,对实验动物血液和肝组织脂质指标和脂质过氧化指标进行检测,并对动物肝脏进行病理组织学观察。结果 经口给予CES 10~90 mg/kg两周,可降低高血脂金黄地鼠血清和肝脏组织中血清总胆固醇（TC）,甘油三酯（TG）和低密度脂蛋白胆固醇（LDL-c）含量（P<0.05或P<0.01）;经口给予高血脂家兔CES 6~24.0 mg/kg,给药10 d时,可降低血清TC和LDL-c含量（P<0.01）;给药20 d和30 d,不仅降低了血清TC、LDL-c含量（P<0.01）,还降低了TG含量（P<0.05）,表现出作用持续时间长而平稳的特点。同时,CES还可降低肝脏组织中TC、TG含量（P<0.05）和丙二醛（MDA）、血清脂肪酶（LPS）含量（P<0.05）。病理组织学观察显示：家兔模型组肝细胞胞浆内脂肪堆积明显,肝细胞受损程度严重,有大面积点状坏死现象。随着CES给药剂量的增加,肝细胞胞浆内脂肪堆积明显减少,肝细胞受损程度也明显减轻。结论 CES对动物高血脂脂代谢紊乱有明显治疗作用,其对高血脂脂代谢紊乱的治疗作用可能与其降低肝组织中MDA和LPS的含量有关。     

Antidiabetic activity of Diospyros peregrina fruit: Effect on hyperglycemia, hyperlipidemia and augmented oxidative stress in experimental type 2 diabetes

Diospyros peregrina is an edible fruit of costal West-Bengal. The present investigation was undertaken to evaluate the role of aqueous extract of D. peregrina fruit in streptozotocin–nicotinamide induced type 2 diabetic rats. Oral administration of extract at the doses of 50 and 100 mg/kg body weight per day for 28 days to diabetic rats was found to possess significant dose dependant hypoglycemic and hypolipidemic activity. An increased reactive oxygen species and insufficient antioxidant activity is associated with diabetes mellitus, which is mainly responsible for diabetic pathogenesis. The role of extract on antioxidant markers of liver and kidney were estimated. The diabetic rats exhibited lower activities of superoxide dismutase (SOD), catalase (CAT), and reduced glutathione (GSH) content in hepatic and renal tissues as compared with normal rats. The activities of SOD, CAT, and GSH were found to be increased in extract treated diabetic rats in selected tissues. The increased level of lipid peroxidation (thiobarbituric acid reactive substances and hydroperoxide) in diabetic rats was also found to be reverted back to near normal status in extract treated groups.     

Hepatoprotective and antioxidant activity of Leucas aspera against d-galactosamine induced liver damage in rats

Context: Whole plant of Leucas aspera (LA) Willd. (Labiatae) is traditionally used in Siddha medicine for hepatic ailments.

Objective: LA was investigated for its hepatoprotective, antioxidant, and protective effect on microsomal drug metabolizing enzymes (MDMEs).

Materials and methods: LA aqueous extract (200 and 400 mg/kg, p.o.) was evaluated for its hepatoprotective and antioxidant activity in d-galactosamine (d-GalN)-induced hepatotoxicity in rats. Biochemical and histopathological studies were performed to assess hepatoprotective activity. Hexobarbitone-induced sleeping time model was used to study the protective effect of LA on MDMEs.

Results: d-GalN administration induced hepatotoxicity in rats which was manifested by increased levels of alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, total cholesterol, triglycerides, total bilirubin and oxidative stress. Pretreatment with LA extract significantly protected the liver in d-GalN administered rats. LA extract significantly elevated antioxidant enzymes like superoxide dismutase, catalase, glutathione peroxidase and decreased lipid peroxidation levels in liver. The total phenolic and flavonoid content in LA aqueous extract was found to be 28.33 ± 0.19 gallic acid equivalents mg/g of extract and 3.96 ± 0.57 rutin equivalent mg/g of extract, respectively. LA extract (200 and 400 mg/Kg) treatment with CCl₄ decreased the hexobarbitone-induced sleeping time in mice by 56.67 and 71.30%, respectively, which indicated the protective effect of LA on hepatic MDMEs. Histological studies showed that LA at 400 mg/kg attenuated the hepatocellular necrosis in d-GalN intoxicated rats.

Conclusion: Our results contribute towards validation of the traditional use of LA in hepatic disorders.     

Ameliorative effect of polyphenols from Padina boergesenii against ferric nitrilotriacetate induced renal oxidative damage: With inhibition of oxidative hemolysis and in vitro free radicals

The aim of this study was to evaluate the antioxidant activities of diethyl ether (DEE) and methanol (M) extracts from brown alga Padina boergesenii using in vitro and in vivo antioxidant assay, which may help to relate the antioxidant properties with the possible outline of its ameliorative effect. M extract showed higher radical scavenging activity through ferric reducing antioxidant power 139.11 µmol tannic acid equivalent/g; DPPH 71.32 ± 0.56%; deoxyribose radical 88.31 ± 0.47%, and total antioxidant activity 0.47 ± 0.02 mg ascorbic acid equivalents/g. Oxidative red blood cell (RBC) hemolysis inhibition rate was significantly higher in M extract (150 mg/kg body weight) in reference to total phenolic content (r = 0.935). Rats administered with DEE and M extracts (150 mg/kg body weight) for seven days before the administration of ferric nitrilotriacetate (9 mg of Fe/mg/kg bodyweight). Rats pretreated with extracts significantly changed the level of renal microsomal lipid peroxidation, glutathione, and antioxidant enzymes in post‐mitochondrial supernatant (P < 0.05). Ameliorative effect of extracts against renal oxidative damage was evident in rat kidney through changes in necrotic and epithelial cells. HPTLC technique has identified the presence of rutin with reference to retardation factor (R_f) in both the extracts. These findings support the source of polyphenols (rutin) from P. boergesenii had potent antioxidant activity; further work on isolation of bioactive compounds can be channeled to develop as a natural antioxidant. © 2014 Wiley Periodicals, Inc. Environ Toxicol 30: 865–876, 2015.     

Andrographolide and kalmegh (Andrographis paniculata) extract: in vivo and in vitro effect on hepatic lipid peroxidation

Single or repeated (for 15 consecutive days) oral administration of kalmegh leaf extract (500 mg/kg) or its bitter principle, andrographolide (5 mg/kg), to adult male albino rats (b.wt. 125-150 g) produced no significant change in NADPH induced hepatic microsomal lipid peroxidation. Carbontetrachloride (5 ml/kg) induced hepatic microsomal lipid peroxidation was decreased when the rats were pretreated (for 4 hr), but only with a single dose and not with long term administration of kalmegh or andrographolide. In vitro carbontetrachloride (1 microliter) induced hepatic microsomal lipid peroxidation was completely normalized by kalmegh leaf extract (0.5 and 5.0 micrograms/mg protein) or andrographolide (0.5 and 5.0 micrograms/mg protein). At the higher concentration of carbontetrachloride (2 microliter), hepatic microsomal lipid peroxidation remained significantly increased (25 %) in the presence of andrographolide (0.5 microgram/mg protein), but not in the presence of kalmegh extract (0.5 microgram/protein). These results suggest that kalmegh leaf extract has more protective action on carbontetrachloride-induced hepatic toxicity than its bitter principle, andrographolide.     

Protection against cisplatin-induced nephrotoxicity in mice by <Emphasis Type="Italic">Curcuma comosa</Emphasis> Roxb. ethanol extract

The protective effect of an ethanol extract of Curcuma comosa against cisplatin-induced renal toxicity in mice was studied. Adult male mice were pretreated for 4 days with the ethanol extract of C. comosa [100–200 mg/kg body weight (BW), orally (p.o.)] before injection of cisplatin (12.5 mg/kg BW, intraperitoneally (i.p.)). Five days later the mice were killed, and blood samples were collected to determine blood urea nitrogen (BUN) and plasma creatinine levels. Kidneys were examined histopathologically and levels of lipid peroxidation, gluthathione (GSH) content, and superoxide dismutase (SOD), gluthathione peroxidase (GPx), and catalase (CAT) activities were determined. Histological examinations revealed degenerative changes and tubular necrosis in mice treated with cisplatin, which were improved by pretreatment with C. comosa ethanol extract. Cisplatin raised BUN, creatinine, and kidney lipid peroxidation levels, and lowered kidney GSH content and levels of GPx, SOD, and CAT activities, all of which (except SOD and CAT) could be restored to normal values by pretreatment with 200 mg/kg BW of C. comosa ethanol extract. In addition, the ethanol extract of C. comosa and its isolated diarylheptanoid compound also exhibited radical scavenging activities. The results suggest that the ethanol extract of C. comosa exhibits effective protection against cisplatin-induced nephrotoxicity mediated through its antioxidant activity.     

绿原酸对肝纤维化大鼠脂质过氧化作用的影响

目的 研究绿原酸（CGA）对肝纤维化大鼠脂质过氧化作用的影响.方法 采用皮下注射CCl4诱导大鼠肝纤维化,以绿原酸（100 mg/kg）同时灌服给药8周,检测对照组、模型组和绿原酸组大鼠血清、肝组织中丙二醛（MDA）含量和超氧化物歧化酶（SOD）活性,病理检测肝纤维化进展.结果 绿原酸能显著降低肝纤维化大鼠血清、肝组织中MDA含量,提高SOD的活性,抑制肝纤维化形成.结论 绿原酸具有很明显的保护肝细胞、抗肝纤维化的作用,其机制可能与抗脂质过氧化有关.     

Garlic extract inhibits the enhanced peroxidation and production of lipids in carbon tetrachloride-induced liver injury

Carbon tetrachloride (CCl4) enhances lipid peroxidation, resulting in triglyceride accumulation in the liver. In this report, we studied the therapeutic, but not the preventive, effect of garlic extract on CCl4-intoxicated liver, in comparison to the effect of vitamin E. Garlic extract was given orally to mice in the dose of 10, 100 or 500 mg/kg at 6 hr after CCl4 administration. The increased conjugated-diene level was diminished significantly to 82% by the 100 mg/kg extract, and also thiobarbituric acid-reactivity was inhibited by all the doses of the extract. In addition to the above mentioned effects, the high doses of garlic extract lowered hepatic triglyceride and lipid contents. Highly significant and positive correlation was observed between hepatic triglyceride content and conjugated-diene level in the lipid fraction of the liver. Besides, vitamin E at the dose of 25 mg/kg inhibited only lipid peroxidation. We, therefore, conclude that not only is garlic extract effective on diminution of lipid peroxide and on alteration of peroxidative status to more reductive condition like the effect of vitamin E, but it also inhibits hepatic triglyceride accumulation in injured liver.     

Studies on protective effect of DA-9601,Artemisia asiatica extract, on acetaminophen- and CCI4-induced liver damage in rats

The hepatoprotective effect of DA-9601, a quality-controlled extract ofArtemisia asiatica, on liver damage induced by acetaminophen (APAP) and carbon tetrachloride (CCI₄) was investigated by means of serum-biochemical, hepatic-biochemical, and histopathological examinations. Doses of DA-9601 (10, 30, or 100mg/kg) were administered intragastrically to each rat on three consecutive days i.e. 48 h, 24 h and 2 h before a single administration of APAP (640 mg/kg, i.p.) or CCl₄ (2 ml/kg, p.o.). Four h and 24 h after hepatotoxin treatment, the animals were sacrificed for evaluation of liver damage. Pretreatment of DA-9601 reduced the elevation of serum ALT, AST, LDH and histopathological changes such as centrilobular necrosis, vacuolar degeneration and inflammatory cell infiltration dose-dependently. DA-9601 also prevented APAP- and CCl₄-induced hepatic glutathione (GSH) depletion and CCl₄-induced increase of hepatic malondialdehyde (MDA), a parameter of lipid peroxidation, in a dose-dependent manner. These findings suggest that pretreatment with DA-9601 may reduce chemically induced liver injury by complex mechanisms which involve prevention of lipid peroxidation and preservation of hepatic GSH.     

Water and Ethanol Extracts of Piper nigrum in Regulating Thyroid Function and Lipid Peroxidation in Mice

Abstract

An investigation was made to evaluate the effects of water and ethanol extracts of Piper nigrum L. fruits in the alteration of the serum thyroid hormone concentrations and tissue lipid peroxidation in liver, the main target organ of many drugs. The alcohol extract, at a dose of 4.0 mg/kg for 15 days, caused thyrotoxicosis as evidenced by increased concentrations of thyroxine and triiodothyronine. A concomitant increase in hepatic lipid peroxidation with a decrease in superoxide dismutase and/or catalase activities also indicated its peroxidative effect. However, a trial with the aqueous extract did not exhibit any toxic effect either on thyroid or in liver functions. Rather, the latter extract appeared to be antithyroidic and antiperoxidative in nature as it could decrease serum thyroid hormone concentrations and hepatic lipid peroxidation, respectively. It is suggested that the aqueous extract of Piper nigrum may be preferred over the alcohol extract for therapeutic uses.     

熊果酸和齐墩果酸抗肝脂肪变和纤维化作用研究进展

熊果酸和齐墩果酸的抗氧化作用能对抗各种原因引起的氧化应激所致的肝组织脂质过氧化反应、炎性损伤、脂肪变和纤维化。熊果酸和齐墩果酸通过阻断两面神激酶2-信号传导及转录激活因子3（JAK2-STAT₃）信号转导,抑制还原型烟酰胺腺嘌呤二核苷酸磷酸氧化酶（NOX）活化,阻止静息态肝星状细胞活化、增殖,促进活化态肝星状细胞凋亡,从而减少胶原生成、增加细胞外基质降解,产生防治肝纤维化的作用。熊果酸和齐墩果酸诱导肝脏去毒酶和外排转运体表达,降低胆汁淤积动物血清胆汁酸、胆红素水平和肝脏胆汁酸水平,减轻胆汁淤积性肝损伤和纤维化;还可通过降血脂作用抑制肝外脂质在肝脏沉积、抑制肝脏脂质生物合成和促进脂质代谢,阻滞肝脂肪变的发生和发展。     

双环醇对四环素诱发小鼠急性脂肪肝的保护作用

研究双环醇对四环素诱发小鼠急性脂肪肝的影响。小鼠一次腹腔注射四环素(180 mg·kg^-1) 24 h后，收集血样和肝组织，采用生化法测定肝脏甘油三酯(triglyceride，TG)、胆固醇(cholesterol，CHO)、谷胱甘肽(glutathione，GSH)含量，以及血清脂质和转氨酶水平；光谱法测定小鼠线粒体脂肪酸β-氧化速率以及肝脏极低密度脂蛋白(very low density lipoprotein，VLDL，TG)分泌速率。结果表明，双环醇(150及300 mg·kg^-1)连续灌胃给药3次可以不同程度地保护四环素引起的小鼠肝脏TG和CHO升高以及血清谷丙转氨酶(alanine aminotransferase，ALT)、谷草转氨酶(aspartate aminotransferase，AST)升高和脂质异常。双环醇(300 mg·kg^-1)还可减轻四环素诱发小鼠肝脏丙二醛(malondialdehyde，MDA)生成增加和GSH水平降低，并能抑制肝线粒体脂肪酸β-氧化速率下降。双环醇(300 mg·kg^-1)可部分逆转四环素所致小鼠肝脏VLDL(TG)分泌速率的减少。由此可见，双环醇对四环素诱发小鼠急性脂肪肝具有明显的保护作用，其作用机制与保护肝线粒体β-氧化功能、改善肝脂蛋白分泌及转运以及抑制肝脏脂质过氧化密切相关。     

Effectiveness of Amygdalus mongolica oil in hyperlipidemic rats and underlying antioxidant processes

The seeds of Amygdalus mongolica contain various constituents including flavonoids and vitamin E, which are known to exert antioxidant effects. However, the safety of the oil extract of this compound is not fully known. The aim of this study was to determine the physicochemical properties of A. mongolica oil, identify the constituents and subsequently assess the effectiveness of utilizing this seed extract in hyperlipidemia as an antioxidant agent. In particular, the toxicity and safety of A. mongolica oil were examined with emphasis on effects on blood lipids level and serum lipid peroxidation using a hyperlipidemia rat model. Treatment with 20 ml/kg A. mongolica oil produced no apparent adverse effects after 14 days in normal female and male rats. A dose of 2.5–10 ml/kg A. mongolica oil administered to hyperlipidemic male rats significantly decreased serum total cholesterol (TC), low-density lipoprotein-C (LDL-C), malondialdehyde (MDA), total cholesterol high-density lipoprotein-C (TC/HDL-C), LDL-C/HDL-C, and atherosclerosis index(AI). In contrast, glutathione (GSH) levels and activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) were significantly increased. Data demonstrated that A. mongolica oil may be utilized in conditions of hyperlipidemia due to its antioxidant effects.     

Antinociceptive Properties of the Hydroalcoholic Extract and the Flavonoid Rutin Obtained from Polygala paniculata L. in Mice

Abstract: The present study examined the antinociceptive effects of a hydroalcoholic extract of Polygala paniculata in chemical and thermal behavioural models of pain in mice. The antinociceptive effects of hydroalcoholic extract was evaluated in chemical (acetic‐acid, formalin, capsaicin, cinnamaldehyde and glutamate tests) and thermal (tail‐flick and hot‐plate test) models of pain or by biting behaviour following intratecal administration of both ionotropic and metabotropic agonists of excitatory amino acids receptors glutamate and cytokines such as interleukin‐1β (IL‐1β) and tumour necrosis factor‐α (TNF‐α) in mice. When given orally, hydroalcoholic extract (0.001–10 mg/kg), produced potent and dose‐dependent inhibition of acetic acid‐induced visceral pain. In the formalin test, the hydroalcoholic extract (0.0001–0.1 mg/kg orally) also caused significant inhibition of both the early (neurogenic pain) and the late (inflammatory pain) phases of formalin‐induced licking. However, it was more potent and efficacious in relation to the late phase of the formalin test. The capsaicin‐induced nociception was also reduced at a dose of only 1.0 mg/kg orally. The hydroalcoholic extract significantly reduced the cinnamaldehyde‐induced nociception at doses of 0.01, 0.1 and 1.0 mg/kg orally. Moreover, the hydroalcoholic extract (0.001–1.0 mg/kg orally) caused significant and dose‐dependent inhibition of glutamate‐induced pain. However, only rutin, but not phebalosin or aurapten, isolated from P. paniculata, administered intraperitoneally to mice, produced dose‐related inhibition of glutamate‐induced pain. Furthermore, the hydroalcoholic extract (0.1–100 mg/kg orally) had no effect in the tail‐flick test. On the other hand, the hydroalcoholic extract caused a significant increase in the latency to response at a dose of 10 mg/kg orally, in the hot‐plate test. The hydroalcoholic extract (0.1 mg/kg orally) antinociception, in the glutamate test, was neither affected by intraperitoenal treatment of animals with l ‐arginine (precursor of nitric oxide, 600 mg/kg) and naloxone (opioid receptor antagonist, 1 mg/kg.) nor associated with non‐specific effects such as muscle relaxation or sedation. In addition, oral administration of hydroalcoholic extract produced a great inhibition of the pain‐related behaviours induced by intrathecal injection of glutamate, N‐methyl‐d ‐aspartate (NMDA), IL‐1β and TNF‐α, but not by α‐amino‐3‐hydroxy‐5‐methyl‐isoxazole‐4‐propionic acid (AMPA), kainate or trans‐1‐amino‐1.3‐cyclopentanediocarboxylic acid (trans‐ACPD). Together, our results suggest that inhibition of glutamatergic ionotropic receptors, may account for the antinociceptive action reported for the hydroalcoholic extract from P. paniculata in models of chemical pain used in this study.