瑞香素对血清脂质及脂蛋白胆固醇含量的影响

Daphnetin is one of the components of Daphne koreana Nakai and the sample used in the experiment is the synthesized product. The compound was shown to possess obvious effect on lipid and lipoprotein cholesterol contents in the serum of normal and hyperlipidemic mice or rats. When daphnetin was given orally to rats, the serum level of high density lipoprotein cholesterol and the ratio of high density lipoprotein cholesterol to total cholesterol of normal rats were raised, whereas no significant effect on the level of lipid in normal mice was observed. Daphnetin (800 mg/kg, po for 1 week) decreased significantly the total cholesterol content in the serum of yolk(0.5 ml) treated mice. In addition, when daphnetin was given orally at a dosage of 800 mg/kg day for 2 weeks, the serum level of total cholesterol decreased. The sernm concentration of high density lipoprotein cholesterol and the ratio of high density lipoprotein cholesterol to total cholesterol in rats with hyperlipidemia increased significantly.     

瑞香素对血清脂质及脂蛋白胆固醇含量的影响

瑞香素(daphnetin)系瑞香科植物长白瑞香(Daphne koreana Nakai)中的有效单体,化学结构为7,8-二羟基香豆素,并已由长春春城制药厂人工合成。药理实验证明有扩张冠状血管、增加冠脉流量,改善心肌代谢作用,并有抑制实验性“关节炎”及兴奋垂体—肾上     

Safety assessment of a new multivitamin

A newly created multivitamin possesses many protective health functions. To investigate its safety when applied in medical treatment and when used as a food supplement, we studied its acute oral toxicity and 13-week oral toxicity in mice. The results showed that the oral lethal dose, 50% (LD₅₀) of the biomass of the multivitamin in mice was greater than 2492 mg/kg body weight (BW) and that poisoned mice recovered within 72 h. The no observed effect level (NOEL) of long-term consumption was more than 249.3 mg/kg BW for haematological parameters, clinical chemistry parameters, histopathological examination of organs, food consumption, BW, ratio of organ weight to BW and other physiological parameters and conditions. Therefore, we conclude that dosages of up to 249.3 mg/kg BW/day of this multivitamin do not cause chronic toxicity in animals. Administration of this multivitamin may even improve the resistance of animals to negative environmental factors and may be safe for long-term consumption to enhance the health of individuals in accordance with the prescribed dosage (1.4 ∼ 4.2 mg/kg BW/day).     

Deltamethrin-induced oxidative damage and biochemical alterations in rat and its attenuation by Vitamin E

Deltamethrin is a synthetic pyrethroid insecticide used worldwide in agriculture, home pest control, protection of foodstuff and disease vector control. The objective of this study was to investigate the propensity of deltamethrin to induce oxidative stress and changes in biochemical parameters and enzyme activities in male rats following a short-term (30 days) oral exposure and its possible attenuation by Vitamin E (Vit. E). Rats were assigned to 1 of 4 treatment groups: 0mg Vit. E and 0mg deltamethrin/kg body weight (BW) (control); 100mg Vit. E/kg BW; 1.28mg deltamethrin/kg BW; 100mg Vit. E plus 1.28mg deltamethrin/kg BW. Results obtained showed that deltamethrin significantly (P<0.05) induced thiobarbituric acid-reactive substances (TBARS; the marker of lipid peroxidation) in plasma. The activities of glutathione S-transferase (GST) and superoxide dismutase (SOD) were significantly decreased due to deltamethrin administration. On the other hand, treatment with Vitamin E alone increased the activities of GST and SOD, and decreased the levels of TBARS. Also, Vitamin E alleviated the harmful effect of deltamethrin in the combination group. Enzymatic activities of aminotransferases (AST and ALT), phosphatases (AcP and AlP) and lactate dehydrogenase (LDH) in plasma were significantly increased, while acetylcholinesterase (AChE) was inhibited. Deltamethrin significantly (P<0.05) increased the levels of plasma total lipid (TL), cholesterol, triglyceride (TG), low density lipoprotein (LDL) and very low density lipoprotein (VLDL), while the level of high density lipoprotein (HDL) decreased. Vitamin E alone decreased the levels of lipids and lipoproteins, and alleviated the harmful effects of deltamethrin. Concentrations of glucose, urea, creatinine and total bilirubin were increased. While, plasma total protein (TP), albumin (A) and globulin (G) were significantly (P<0.05) decreased. The present study revealed that the presence of Vitamin E could diminish the adverse effects of deltamethrin on most of biochemical parameters, lipid peroxidation and enzyme activities in rats.     

Ameliorative effect of sesame lignans on nicotine toxicity in rats

Nicotine causes oxidative and genotoxic damages in the tissues leading to several diseases. Any strategy through natural diet that prevents or slows the progression and severity of nicotine toxicity has a significant health impact. This work is designed to investigate natural antioxidants that play effective protective role against nicotine-induced toxicity. Experiments were conducted on male albino rats by injecting nicotine tartrate (3.5 mg/kg body wt./day for 15 days) subcutaneously and thereby supplementing sesame lignans (0.1 g/100 g diet and 0.2 g/100 g diet) orally to them. Significant (P < 0.01) increase of total cholesterol, triglyceride, LDL-cholesterol, VLDL-cholesterol, decrease of HDL-cholesterol, decrease in antioxidant enzymes and increase in concentration of lipid peroxidative product has been observed in plasma due to nicotine toxicity. Significant (P < 0.01) decrease of total DNA contents and highly significant (P < 0.001) DNA damage of liver tissue is also observed on nicotine treatment. Sesame lignans minimizes the above mentioned effects. The nicotine-induced oxidative and genotoxic damages on the tissues can be effectively attenuated by sesame lignans supplemented diet.     

Impact of short‐term low‐dose atorvastatin on low‐density lipoprotein and high‐density lipoprotein subfraction phenotype

Statins can significantly reduce low‐density lipoprotein–cholesterol (LDL‐C) and modestly raise or not alter high‐density lipoprotein–cholesterol (HDL‐C). However, their impact on high‐density lipoprotein (HDL) and low‐density lipoprotein (LDL) subfractions has been less examined. The aim of the present study was to investigate the short‐term impact of low‐dose atorvastatin on HDL and LDL subfractions in humans. In this randomized study, data from 52 subjects were analysed. Thirty‐seven patients with atherosclerosis were randomized to treatment with atorvastatin 10 mg/day (n = 17) or 20 mg/day (n = 20) for 8 weeks, with 15 healthy subjects without therapy used as a control group. The lipid profile and lipoprotein subfractions were determined using the Lipoprint system at baseline and at 8 weeks. The data suggest that atorvastatin treatment (10 and 20 mg/day) for 8 weeks significantly decreases LDL‐C levels and reduces the cholesterol concentration of all LDL subfractions, which is accompanied by an increase of the mean LDL particle size. Although 10 mg/day atorvastatin treatment for 8 weeks had no impact on the HDL subfraction, 20 mg/day atorvastatin for 8 weeks significantly increased the cholesterol concentration of large HDL particles and decreased the cholesterol concentration of small HDL particles without changing serum HDL‐C levels in patients with atherosclerosis. Therefore, the results suggest that 20 mg/day atorvastatin treatment for 8 weeks may result in a favourable modification of the HDL subfraction phenotype in addition to its effects on the cholesterol concentration of all LDL subfractions and mean LDL particle size.     

Study of the protective effect of ascorbic acid against the toxicity of stannous chloride on oxidative damage, antioxidant enzymes and biochemical parameters in rabbits

Stannous chloride (SnCl2) is a reducing chemical agent used in several man-made products. SnCl2 can generate reactive oxygen species (ROS). Therefore, the present study has been carried out to investigate the antioxidant action of l-ascorbic acid (AA) in minimizing SnCl2 toxicity on lipid peroxidation, antioxidant enzyme, and biochemical parameters in male New Zealand white rabbits. Animals were assigned to one of four treatment groups: 0mg AA and 0mg SnCl2/kg BW (control); 40 mg AA/kg BW; 20mg SnCl2/kg BW; 20mg SnCl2 plus 40 mg AA/kg BW. Rabbits were orally administered the respective doses every other day for 12 weeks. Results obtained showed that SnCl2 significantly (P<0.05) induced thiobarbituric acid-reactive substances (TBARS; the marker of lipid peroxidation) in plasma, while the activities of glutathione S-transferase (GST), superoxide dismutase (SOD) and catalase (CAT), and the level of sulfhydryl groups (SH-group) were decreased (P<0.05) in blood plasma. Aspartate transaminase (AST), alanine transaminase (ALT), alkaline phosphatase (AlP), acid phosphatase (AcP) and lactate dehydrogenase (LDH) activities were decreased (P<0.05). Stannous chloride significantly (P<0.05) increased the levels of plasma total lipid (TL), cholesterol, triglyceride (TG), low-density lipoprotein (LDL) and very low-density lipoprotein (VLDL), glucose, urea and total bilirubin. On the other hand, the level of plasma high-density lipoprotein (HDL), total protein (TP), albumin (A) and globulin (G) were significantly (P<0.05) decreased. Ascorbic acid alone significantly decreased the levels of TBARS, lipids and urea, and increased the activities of GST, SOD and CAT, and the levels of SH-group and proteins. While the rest of the tested parameters were not affected. Also, the presence of AA with SnCl2 alleviated its harmful effects on most of the tested parameters. Therefore, the present results revealed that treatment with AA could minimize the toxic effects of stannous chloride.     

Chrysin alleviates testicular dysfunction in adjuvant arthritic rats via suppression of inflammation and apoptosis: Comparison with celecoxib

Long standing rheumatoid arthritis (RA) is associated with testicular dysfunction and subfertility. Few studies have addressed the pathogenesis of testicular injury in RA and its modulation by effective agents. Thus, the current study aimed at evaluating the effects of two testosterone boosting agents; chrysin, a natural flavone and celecoxib, a selective COX-2 inhibitor, in testicular impairment in rats with adjuvant arthritis, an experimental model of RA. Chrysin (25 and 50 mg/kg) and celecoxib (5 mg/kg) were orally administered to Wistar rats once daily for 21 days starting 1 h before arthritis induction. Chrysin suppressed paw edema with comparable efficacy to celecoxib. More important, chrysin, dose-dependently and celecoxib attenuated the testicular injury via reversing lowered gonadosomatic index and histopathologic alterations with preservation of spermatogenesis. Both agents upregulated steroidogenic acute regulatory (StAR) mRNA expression and serum testosterone with concomitant restoration of LH and FSH. Furthermore, they suppressed inflammation via abrogation of myeloperoxidase, TNF-α and protein expression of COX-2 and iNOS besides elevation of IL-10. Alleviation of the testicular impairment was accompanied with suppression of oxidative stress via lowering testicular lipid peroxides and nitric oxide. With respect to apoptosis, both agents downregulated FasL mRNA expression and caspase-3 activity in favor of cell survival. For the first time, these findings highlight the protective effects of chrysin and celecoxib against testicular dysfunction in experimental RA which were mediated via boosting testosterone in addition to attenuation of testicular inflammation, oxidative stress and apoptosis. Generally, the 50 mg/kg dose of chrysin exerted comparable protective actions to celecoxib.     

Chrysin protects against cisplatin-induced colon. toxicity via amelioration of oxidative stress and apoptosis: probable role of p38MAPK and p53

Cisplatin, an antineoplastic drug, is widely used as a foremost therapy against numerous forms of cancer but it has pronounced adverse effects viz., nephrotoxicity, ototoxicity etc. CDDP-induced emesis and diarrhea are also marked toxicities that may be due to intestinal injury. Chrysin (5,7-dihydroxyflavone), a natural flavone commonly found in many plants possesses multiple biological activities, such as antioxidant, anti-inflammatory and anti-cancer effects. In the present study, we investigated the protective effect of chrysin against CDDP-induced colon toxicity. The plausible mechanism of CDDP-induced colon toxicity and damage includes oxidative stress, activation of p38MAPK and p53, and colonic epithelial cell apoptosis via upregulating the expression of Bak and cleaved caspase-3. Chrysin was administered to Wistar rats once daily for 14 consecutive days at the doses of 25 and 50 mg/kg body weight orally in corn oil. On day 14, a single intraperitoneal injection of cisplatin was given at the dose of 7.5 mg/kg body weight and animals were euthanized after 24 h of cisplatin injection. Chrysin ameliorated CDDP-induced lipid peroxidation, xanthine oxidase activity, glutathione depletion, decrease in antioxidant (catalase, glutathione reductase, glutathione peroxidase and glucose-6 phosphate dehydrogenase) and phase-II detoxifying (glutathione-S-transferase and quinone reductase) enzyme activities. Chrysin also attenuated goblet cell disintegration, expression of phospho-p38MAPK and p53, and apoptotic tissue damage which were induced by CDDP. Histological findings further supported the protective effects of chrysin against CDDP-induced colonic damage. The results of the present study suggest that the protective effect of chrysin against CDDP-induced colon toxicity was related with attenuation of oxidative stress, activation of p38MAPK and p53, and apoptotic tissue damage.     

Ameliorative role of conjugated linolenic acid isomers against oxidative DNA damage induced by sodium arsenite in rat model

The present study was undertaken to evaluate the ameliorative role of α-eleostearic acid and punicic acid, isomers of conjugated linolenic (CLnA) acid, against oxidative stress induced DNA damage. Male albino rats were divided into six groups. Group 1 and 2 were normal control and sodium arsenite treated (Sa; 10 mg/kg BW) control respectively. Group 3–6 were orally treated with different doses of two fatty acids (0.5% and 1.0% of total lipid given for each isomer) along with sodium arsenite (Sa; 10 mg/kg BW). Comet assay of blood leukocytes showed that administration of CLnA reduced DNA damage significantly (P < 0.05) which was determined by tail DNA percent and olive tail moment. Results showed that activity of antioxidant enzymes viz. catalase, superoxide dismutase (SOD), glutathione peroxidase (GPx) and reduced glutathione (GSH) in plasma, liver and erythrocyte lysate decreased and activity of nitric oxide synthase in plasma and liver increased significantly due to oxidative stress generated by sodium arsenite. Administration of CLnA isomers restored all the altered parameters and also reduced lipid peroxidation and leakage of transaminase enzymes from liver to blood due to liver injury. α-Eleostearic acid was more efficient antioxidant than punicic acid against oxidative DNA damage.     

Atherosclerosis induced by arsenic in drinking water in rats through altering lipid metabolism

Arsenic in drinking water is a global environmental health problem, and the exposure may increase cardiovascular and cerebrovascular diseases mortalities, most likely through causing atherosclerosis. However, the mechanism of atherosclerosis formation after arsenic exposure is still unclear. To study the mechanism of atherosclerosis formation after arsenic exposure and explore the role of high cholesterol diet (HCD) in this process, we fed spontaneous hypertensive rats and Wistar Kyoto rats with basal diet or HCD and provided with them drinking water containing arsenic at different ages and orders for 20 consecutive weeks. We measured high density lipoprotein cholesterol (HDL-C), low density lipoprotein cholesterol (LDL-C), total cholesterol, triglycerides, heat shock protein 70 (HSP 70), and high sensitive C-reactive protein (hs-CRP) at predetermined intervals and determined expressions of cholesteryl ester transfer protein-1 (CETP-1) and liver X receptor β (LXRβ) in the liver. Atherosclerosis was determined by examining the aorta with hematoxylin and eosin stain. After 20 weeks, we found arsenic, alone or combined with HCD, may promote atherosclerosis formation with transient increases in HSP 70 and hs-CRP. Early combination exposure decreased the HDL-C/LDL-C ratio without changing the levels of total cholesterol and triglyceride until 30 weeks old. Both CETP-1 and LXRβ activities were suppressed, most significantly in early combination exposure. In conclusion, arsenic exposure may induce atherosclerosis through modifying reverse cholesterol transport in cholesterol metabolism and suppressing LXRβ and CEPT-1 expressions. For decreasing atherosclerosis related mortality associated with arsenic, preventing exposure from environmental sources in early life is an important element.     

Chrysin abrogates early hepatocarcinogenesis and induces apoptosis in N-nitrosodiethylamine-induced preneoplastic nodules in rats

Flavonoids possess strong anti-oxidant and cancer chemopreventive activities. Chrysin (5,7-dihydroxyflavone) occurs naturally in many plants, honey, and propolis. In vitro, chrysin acts as a general anti-oxidant, causes cell cycle arrest and promotes cell death. However, the mechanism by which chrysin inhibits cancer cell growth and the subcellular pathways activated remains poorly understood. Effect of dietary supplementation with chrysin on proliferation and apoptosis during diethylnitrosamine (DEN)-induced early hepatocarcinogenesis was investigated in male Wistar rats. To induce hepatocarcinogenesis, rats were given DEN injections (i.p., 200 mg/kg) three times at a 15 day interval. An oral dose of chrysin (250 mg/kg bodyweight) was given three times weekly for 3 weeks, commencing 1 week after the last dose of DEN. Changes in the mRNA expression of COX-2, NFkB p65, p53, Bcl-xL and β-arrestin-2 were assessed by quantitative real-time PCR. Changes in the protein levels were measured by western blotting. Chrysin administration significantly (P < 0.001) reduced the number and size of nodules formed. Also, a significant (P < 0.01) reduction in serum activities of AST, ALT, ALP, LDH and γGT was noticed. Expression of COX-2 and NFkB p65 was significantly reduced whereas that of p53, Bax and caspase 3 increased at the mRNA and protein levels. Likewise, a decrease in levels of β-arrestin and the anti-apoptotic marker Bcl-xL was also noted. These findings suggest that chrysin exerts global hepato-protective effect and its chemopreventive activity is associated with p53-mediated apoptosis during early hepatocarcinogenesis.     

Prophylactic effect of α-linolenic acid and α-eleostearic acid against MeHg induced oxidative stress,DNA damage and structural changes in RBC membrane

The present study was undertaken to evaluate under in vivo condition the effects of α-linolenic acid and α-eleostearic acid against methyl mercury (MeHg) induced oxidative stress. Male albino rats were divided into six groups. Group 1 was under normal control and Group 2 was treated with methyl mercury chloride (MeHgCl; 5 mg/kg BW/day). Groups 3, 4, 5 and 6 were orally treated with different doses of the two fatty acids (0.5% and 1.0% of total lipid given for each kind of linolenic acid isomer) along with MeHgCl (5 mg/kg BW). Comet assay of blood lymphocytes showed that administration of α-linolenic acid reduced DNA damage significantly (P < 0.05). Results also showed that activity of antioxidant enzymes of plasma and brain tissue and total antioxidant capacity in plasma decreased significantly due to oxidative stress generated by MeHgCl. Administration in higher dose of both kind of linolenic acid restored all the activities of the antioxidant enzymes and also reduced lipid peroxidation and increased total antioxidant capacity in plasma. Both kinds of linolenic acid successfully maintained the RBC membrane integrity which was totally disrupted and became flat due to MeHgCl stress. α-Linolenic acid was more efficient antioxidant than α-eleostearic acid against oxidative DNA damage.     

Two generation reproduction and teratogenicity studies of feeding cyadox in Wistar rats

To investigate the teratogenic potential and reproductive toxicity of cyadox, a growth promoting agent, Wistar rats (F₀) were fed with diets containing cyadox (0, 50, 150 and 2500 mg/kg) or olaquindox (150 mg/kg), approximately equivalent to cyadox 5, 15, 250 or olaquindox 15 mg/kg b.w./day across two generations. Half of the pregnant rats (F₀, F_1b) were subjected to caesarean section on gestational day 20 for teratogenic examination and the other half produced pups F_1a and F_2a, respectively. At the 250 mg/kg b.w./day cyadox group, body weights of F_1b pregnant rats and F_2a on day 21 after birth decreased; fetal body lengths and tail lengths decreased; the number of fetal resorptions increased significantly; litter weights, number of viable fetuses decreased; number of embryo resorptions increased significantly; number of liveborn F_1a, F_1b and F_2a decreased. No macroscopic or microscopic change of any significance was found in the reproductive organs. Significant increases in the incidence of cervial ribs or lumbar ribs in F_2a pups and significant increases of relative organ weight of testis and epididymis in F_1b were observed at the 250 mg/kg b.w./day cyadox group. The NOAEL for reproduction/development of cyadox for rats was estimated to be 150 mg/kg diet, which was equivalent to approximately 15 mg/kg b.w./day.     

Propolis alleviates aluminium-induced lipid peroxidation and biochemical parameters in male rats

Aluminium is present in many manufactured foods and medicines and is also added to drinking water during purification purposes. Therefore, the present experiment was undertaken to determine the effectiveness of propolis in alleviating the toxicity of aluminium chloride (AlCl₃) on biochemical parameters, antioxidant enzymes and lipid peroxidation of male Wistar Albino rats. Animals were assigned to 1 of 4 groups: control; 34 mg AlCl₃/kg bw; 50 mg propolis/kg bw; AlCl₃ (34 mg/kg bw) plus propolis (50 mg/kg bw), respectively. Rats were orally administered their respective doses daily for 70 days. The levels of thiobarbituric acid reactive substances (TBARS) was increased, and the activities of glutathione S-transferase, superoxide dismutase, catalase and glutathione peroxidase were decreased in liver, kidney and brain of rats treated with AlCl₃. While, TBARS was decreased and the antioxidant enzymes were increased in rats treated with propolis alone. Plasma transaminases, lactate dehydrogenase, glucose, urea, creatinine, bilirubin, total lipid, cholesterol, triglyceride and LDL-c were increased, while total protein, albumin and high HDL-c were decreased due to AlCl₃ administration. The presence of propolis with AlCl₃ alleviated its toxic effects in rats treated with AlCl₃. It can be concluded that propolis has beneficial influences and could be able to antagonize AlCl₃ toxicity.     

Quercetin ameliorates glucose and lipid metabolism and improves antioxidant status in postnatally monosodium glutamate-induced metabolic alterations

We reported the effects of quercetin on metabolic and hormonal profile as well as serum antioxidant activities in a model of MSG (monosodium glutamate)-induced obesity. Rats were divided into 4 groups: MSG group, submitted to neonatal treatment with high doses of MSG, administrated subcutaneously during 10 days, from 2 day-old; control groups, which received the same volume of saline. After completing 30 day-old, these groups were subdivided into 4 groups: control and MSG groups treated and non-treated with quercetin at doses of 75 mg/kg body weight (i.p.) over 42 days. BW gain and food consumption were higher in MSG treated rats and quercetin significantly reduced BW by 25%. While MSG increased triacylglycerol, total cholesterol and fractions, and reduced HDL concentrations, administration of quercetin normalized HDL-cholesterol and reduced others lipids. Insulin, leptin, glucose and creatinine levels were raised in MSG-treated rats and reduced after quercetin treatment. Alanine transaminase, aspartate transaminase, lactate dehydrogenase and alkaline phosphatase activities were lower after MSG-quercetin combination compared to rats given only MSG. MSG-quercetin combination augmented total protein and urea levels as well as glutathione peroxidase and superoxide dismutase activities in contrast to MSG-treated animals. Quercetin normalized serum lipid and glucose profile and minimized the MSG-related toxic effects, which was associated to its antioxidant properties.     

Characterisation and toxicological behaviour of Basic Methacrylate Copolymer for GRAS evaluation

Basic Methacrylate Copolymer is a fully polymerised cationic copolymer with taste-masking and moisture protection properties. It is used as a pharmaceutical excipient and has potential use as a glazing/coating agent to solid food supplements. This article describes available information on the safety of the substance.Oral administration of radiolabelled copolymer to rats showed the major route of excretion to be via the faeces. Minor absorption may occur at <0.02%. Safety studies revealed no adverse toxicity following repeated administration at up to 2000 mg/kg/day in a sub-chronic study in the rat or 750 mg/kg/day in a sub-acute study in the dog. No reproductive toxicity occurred at up to 1000 mg/kg/day in the rat. The substance shows no evidence of genotoxicity, has low acute toxicity and no irritation or sensitisation potential.As per the FDA approach an ADI of 20 mg/kg bw can be concluded. Daily exposure from use as a food additive is estimated as up to 11.7 mg/kg bw in adults and 13.3 mg/kg bw in children. In view of the high molecular weight of the substance, its lack of absorption and its low toxicity profile, the ADI is deemed adequate.     

某些药物对大鼠血浆和肝脏脂蛋白脂酶活性及血浆胆固醇的影响

高浓度极低密度脂蛋白(VLDL)和高浓度低密度脂蛋白(LDL)血症是冠心病的易患因子,脂蛋白脂酶(LPL)可使VLDL转化为LDL,故LPL可能促进动脉粥样斑块的形成。但LPL又可促进高密度脂蛋白(HDL)的生成,而HDL是防止动脉粥样硬化斑块形成的有利因子,故又认为LPL可能有利于防止斑块的生成。由此可见LPL对动脉粥样硬化的影响具有两面性,LPL在脂蛋白代谢中的作用非常复杂。     

某些药物对大鼠血浆和肝脏脂蛋白脂酶活性及血浆胆固醇的影响

Lipoprotein lipase (LPL) is one of the most important factors in lipoprotein metabolism. The plasma and liver LPL activities (indicaded by fatty acid release), the ratio of LPL activity to total lipase activity and theoplasma cholesterol levels in rats treated with drugs were determined so as to study the relationship between LPL and lipoprotein metabolism.Plasma LPL activity is negatively related to the total cholesterol and high density lipoprotein cholesterol levels. As the liver LPL activity, increased, the plasma LPL activity also increased. When rats were treated with insulin, phenytoin or Radix Polygonum multiflorum, the plasma and liver LPL activities and the ratio of LPL activity to total lipase activity increased, whereas the plasma total cholesterol and high density lipoprotein cholesterol levels decreased. No significant effect of phenytoin on the total cholesterol level was observed, When large doses of phenytoin were used, the plasma very low density lipoprotein and low density lipoprotein cholesterol level increased and the ratio of high density lipoprotein cholesterol to total cholesterol decreased.