Role of Huoxue Jiangzhi Recipe in preventing and treating fatty liver in mice

AIM: To explore the role of Huoxue Jiangzhi Recipe in preventing and treating fatty liver in mice and its underlying mechanisms. METHODS: Healthy Kunming mice were fed with high-fat diet and treated intragastrically with different doses of Huoxue Jiangzhi Recipe (compound of ginseng, panax notoginseng and rhizoma gastrodiae, named as GST) for 2 weeks. The levels of blood lipids and triglyceride (TG) in hepatic tissues were measured. Meanwhile, liver index and hepatic pathology were observed. The optimized dosage of Huoxue Jiangzhi Recipe was determined by the experiments. The mice were divided into normal control group (NC group, fed with normal diet) and model group (fed with high-fat diet). The model mice were subdivided into 3 subgroups 12 weeks later: HF group (fed continuously with high-fat diet), ND group (fed with normal diet), GSL group (fed with normal diet and treated intragastrically with GSL). The mice in NC, HF and ND groups were given distilled water by gastric perfusion. Two weeks later, all mice were killed, and blood was collected for measuring serum total cholesterol (TC),TG,high-density lipoprotein-cholesterol (HDL-C), low-density lipoprotein-cholesterol (LDL-C) contents, hepatic TC, TG, malondialdehyde (MDA) levels and superoxide dismutase (SOD) activity were detected. Moreover, liver index and hepatic pathology were also observed. The mRNA expression of peroxisome proliferator-activated receptor alpha (PPARα) and cytochrome-P450 2E1 (CYP2E1) in the liver was examined by RT-PCR. RESULTS: GST significantly decreased serum lipid, hepatic lipid and MDA levels and elevated SOD activity. Furthermore, GST markedly reduced liver index, improved hepatic adipose infiltration, increased PPARα mRNA expression and inhibited CYP2E1 mRNA expression. CONCLUSION: GST is effective in the treatment of fatty liver in mice by up-regulating PPARα, thus reducing serum and hepatic TG levels, down-regulating CYP2E1 and inhibiting lipid peroxidation.     

Effect of bitter melon on liver fibrosis induced by carbon tetrachloride

AIM: To investigate the effects of bitter melon (BM) on liver fibrosis induced by CCl₄ in Wistar rats. METHODS: Healthy male Wistar rats were randomly divided into 4 groups (with 8 each): olive oil control group (group C), olive oil CCl₄ model group (group M), CCl₄+BM at low concentration (BM 100 g/kg, group BM-L), CCl₄+ BM at high concentration (BM 200 g/kg, group BM-H). All rats except those in group C were subcutaneously injected with CCl₄ twice a week for 8 weeks to induce liver fibrosis. After injection of CCl₄ for 8 weeks, all rats were sacrificed and the samples of blood and livers were collected. The weight ratio of liver to body was measured. The serum level of MDA and the activity of SOD were tested. The contents of total protein and albumin, the activity of GSH-Px, the content of hydroxyproline and the activity of monoamine oxidase in the liver homogenate were determined. Hepatic inflammation and collagen deposition were observed under microscope with Masson staining. RESULTS: In the rats treated with BM, the weight ratio of liver to body, the serum level of MDA, the content of hydroxyproline and the activity of monoamine oxidase in the liver homogenate were lower than those in group M (P<0.01). The serum activity of SOD, the contents of total protein and albumin, and the activity of GSH-Px in the liver homogenate were enhanced (P<0.01). The livers of the model rats had remarkable inflammatory necrosis, collagen accumulation and fibrosis. The rats in BM-treated group showed slighter hepatic injury and collagen deposition, and the liver functions were much better than those in the model group. High dose of BM showed more obvious liver-protective effects. CONCLUSION: BM attenuates liver fibrosis by its antioxidant effect and the mechanisms of reducing hydroxyproline content and monoamine oxidase activity.     

Curcumin inhibits lipid peroxidation and the expression of TGF-β1 and PDGF in the liver of rats with hepatic fibrosis

AIM: To investigate changes of the level of reactive oxygen species (ROS),malondialdehyde (MDA),transforming growth factor-β1 (TGF-β1) and platelet-derived growth factor (PDGF) expression in a rat hepatic fibrosis model and the effect of curcumin ,and discuss the mechanism of the prophylactic effect of curcumin on hepa tic fibrosis.METHODS: Rat models of hepatic fibrosis were established by intraperitoneally injection of carbon tetrachloride.Curcumin of 20 mg,10 mg,5mg per 100 gram weight of rat was given to these rats respectively at the same time.Normal,fibrosis model and positive groups were made as controls.After eight weeks,all rats were executed and the blood and liver were kept.Serum level of ROS was tested by chromatometry.Content of MDA in liver homogenate was tested by thiobarbituric acid (TBA) method.Expressions of TGF-β1 and PDGF in liver were detected by immunohistochemical method. RESULTS: Serum level of ROS in fibrotic group increased significantly compared with that of normal group,and which was depressed obviously in curcumin groups(P＜0.05).Content of MDA in liver of curcumin group reduced significantly compared with that of fibrotic group (P＜0.01).Expressions of TGF-β1 and PDGF in fibrotic group increased significantly compared with those of normal group,which were depressed obviously in curcumin groups (P＜0.01).CONCLUSION: Curcumin could inhibit expression of TGF-β1,PDGF and lipid peroxidation in liver.These may be mechanisms of curcumin preventing hepatic fibrosis.     

Riboflavin preconditioning alleviates hepatic ischemia/reperfusion injury in rats

AIM: To explore the protective effect of riboflavin preconditioning on hepatic ischemia/reperfusion injury in rats. METHODS: Twenty-four Sprague-Dawley rats wererandomly divided into 3 groups (n=8): sham group, ischemia/reperfusion (I/R) group and riboflavin preconditioning (R+I/R) group. The rats in sham group and I/R group received a standard chow,while the rats in R+I/R group received a chow supplemented with riboflavin. After 4 weeks, portal vein and hepatic artery supplying the middle and left hepatic lobes were clamped with a traumatic vascular clip for induction of partial hepatic ischemia in the rats in I/R group and R+I/R group. After 1 h of ischemia, 1 h of reperfusion was conducted by removal of the clip. The activity of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) in serum,the activity of superoxide dismutase (SOD) and the level of malondialdehyde (MDA) in serum and liver were measured. Western blotting was employed to examine the protein expression of heme oxygenase-1(HO-1) in the liver. RESULTS: The results showed that ischemia/reperfusion injury markedly increased the activity of AST and ALT in serum, decreased the activity of SOD, and elevated the level of MDA and the activity of HO-1 in the liver as compared with sham group (P<0.01). The riboflavin pretreatment significantly decreased the activity of AST and ALT in serum, increased the activity of SOD and decreased the levels of MDA in serum and liver as compared with I/R group (P<0.01). In addition, the protein expression of HO-1 and the activity of HO-1 were elevated in R+I/R group (P<0.01). Cytoplasmic vacuolation and swelling of the hepatocytes were observed in I/R group. Treatment with riboflavin markedly alleviated the changes of liver structure. CONCLUSION: Riboflavin preconditioning has protective effect on hepatic ischemia/reperfusion injury. The mechanism may be correlated with enhancing the anti-oxidation and alleviating the reaction of lipid peroxidation.     

Effect of salidroside on alcohol-injuced hepatic injury in rats

AIM:To investigate the effect of salidroside on alcoholic hepatic injury in rats. METHODS:The SD rats were randomly divided into 5 groups:negative control group, model group, bifendate group, and low-and high-dose salidroside groups. The rats in model group were administered with 56% alcohol, while the rats in negative control group was administered with saline. The rats in bifendate group and salidroside groups were administered with corresponding drugs every day. The blood and the liver tissues were collected to measure triacylglycerol (TG), alanine aminotransferase (ALT), aspartate aminotransferase (AST), malondialdehyde (MDA) and superoxide dismutase (SOD). The pathological changes of the liver tissues were observed with HE staining. Tumor necrosis factor-α (TNF-α) and nuclear factor-κB (NF-κB) were measured by ELISA and the protein and mRNA expression levels of TNF-α and NF-κB were detected by Western blot and RT-PCR. RESULTS:Compared with model group, the levels of TG, ALT, AST, MDA, TNF-α and NF-κB were reduced, while the activity of SOD was enhanced in salidroside group (P<0.05). The liver tissue injury was significantly attenuated. CONCLUSION:Salidroside improves the pathological changes, reduces inflammation, increases the activity of antioxidant enzymes and reduces lipid peroxidation in the liver with alcohol-induced injury. This effect may be related to regulating the NF-κB-mediated inflammatory responses.     

Changes of gut mucosa antioxidant system and liver,renal function in rats after intestinal ischemia-reperfusion injury

AIM: To investigate the changes of the gut mucosa antioxidant system and liver, renal functions during rat intestinal ischemia-reperfusion injury. METHODS: 30 male Wistar rats underwent 45 min of intestinal ischemia by clamping the superior mesenteric artery followed by reperfusion. The levels of malondialdehyde (MDA), glutathione (GSH), the activities of antioxidant enzymes in the gut mucosa including catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), glutathione S- transferase (GST) activity and serum ALT, AST, BUN, Cr were assayed at 2, 4, 8, 12 and 24 h after reperfusion. RESULTS: The levels of MDA and GSH in the gut mucosa increased and decreased significantly at 2 h of reperfusion, respectively (P<0.05). MDA was still lower than sham at 24 h of reperfusion (P<0.05), while GSH decreased to 40% of sham at 4 h of reperfusion (P<0.01) but returned to the level of control at 12 h. The activities of CAT, SOD and GSH-Px did not show significant changes in rat after intestinal ischemia reperfusion. GST decreased 39% at 2 h of reperfusion compared with the sham group and decreased to 56% of sham at 4 h (P<0.05), but returned to the level of control at 12 h after reperfusion. Serum ALT, AST, BUN and Cr increased significantly at 2 h of reperfusion (P<0.05) and increased 208%, 100%, 103%, 41% compared with control at 4 h of reperfusion (P<0.01). However, at 24 h of reperfusion, they returned to normal. CONCLUSION: Intestinal ischemia/reperfusion diminishes GSH level and GST activity, increases MDA level and causes liver and renal reversible damages.     

The reversal effects of recombinant human augmenter of liver regeneration in immunocomplex induced liver fibrosis

AIM: To observe the anti-fibrosis activity of recombinant human augmenter of liver regeneration (hALR). METHODS: Albumin induced rat model of liver fibrosis was established and hALR was given peritoneally after the model production. Serum concentration of alanine aminotransferase(ALT),aspartic aminotransferase(AST),lactate dehydrogenase(LDH), hepatic collagen contents and pathological examination were selected as observing parameter. RESULTS: Recombinant human augmenter of liver regeneration (hALR) could decrease ALT, AST, LDH concentration of fibrotic rats. The measurements of hepatic collagen contents showed that hepatic collagen contents in hALR treatment group was much lower than those of model group and negative control group. Pathological examination also indicated that the degree of liver fibrosis in hALR treatment group was attenuated in comparison with those of model group and negative control group. CONCLUSION: Recombinant human augmenter of liver regeneration (hALR) had reversal effects on immunocomplex induced rat liver fibrosis.control group. CONCLUSION: Recombinant human augmenter of liver regeneration (hALR) had reversal effects on immunocomplex induced rat liver fibrosis.     

Effects of Anhua dark tea on ApoE-/- mice with non-alcoholic fatty liver induced by high-fat diet

AIM To explore the effects of Anhua dark tea on the prevention and treatment of non-alcoholic fatty liver induced by high-fat diet in apolipoprotein E knockout (ApoE^-/-) mice and the relevant mechanisms. METHODS Male ApoE^-/- mice (n=50, 8 weeks old) were randomly divided into model group, atorvastatin group, and high-, medium- and low-dose Anhua dark tea groups, with 10 mice in each group. In addition, 10 homologous wild-type male C57BL/6J mice were selected as normal control group. The ApoE^-/- and wild-type mice were fed with the same amount of high-fat feed and common feed for 17 weeks, respectively, and intervened by the corresponding drugs and normal saline. At the end of the experiment, HE staining was used to observe the histopathological changes of the liver. The levels of alanine aminotransfease (ALT), aspartate aminotransfease (AST), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and malondialdehyde (MDA) in the liver tissues were detected. The mRNA expression levels of hydroxymethyl glutaryl coenzyme A reductase (HMGCR), peroxisome proliferator-activated receptor-γ (PPAR-γ) and steroyl coenzyme A desaturase-1 （SCD-1） were detected by RT-qPCR to observe the lipid synthesis. RESULTS In model group, increased volume, smooth surface, tight membrane and dull edge of the liver were observed, and microscopic images with HE staining showed the formation of vacuoles with varying sizes, indicating the success of establishing the model. Compared with the model group, the degree of liver steatosis, the levels of ALT, AST and MDA, and the mRNA expression of HMGCR, SCD-1 and PPAR-γ in different doses of Anhua dark tea groups were significantly decreased, while the activity of SOD and GSH-Px was increased (P<0.05). The effect of Anhua dark tea in high- and medium-dose groups was better than that in low-dose group (P<0.05). CONCLUSION Anhua dark tea prevents high-fat diet-induced non-alcoholic fatty liver in ApoE^-/- mice. The mechanism may be related to reducing lipid synthesis by inhibition of HMGCR, SCD-1 and PPAR-γ expression, and protecting liver cells through anti-oxidative activity.     

Mechanisms underlying the protection of berberine against liver injury induced by lipopolysaccharide in mice

AIM: To investigate the protective effects of berberine against liver injury induced by lipopolysaccharide in mice and the mechanisms underlying its protective effect. METHODS: The male mice were divided randomly into control, berberine group, LPS group and berberine treatment group. Mice were administered intragastrically with distilled water (0.01 mL/g) or 5 g/L neutral sulfate berberine (0.01 mL/g) once a day for 5 days and injected intraperitoneally with normal saline or LPS （0.02 mL/g，28 mg/kg）at 1 h after gavage on day 5. Blood was collected for determining alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities, the content of tumor necrosis factors-α (TNF-α) at 10 h and 2 h after LPS or normal saline injection, respectively. Furthermore, the liver tissue was processed, and histological changes and ultrastructure in liver were observed with light and electron microscopy, malondialdehyde (MDA) content and superoxide dismutase (SOD) activity in liver were also detected. RESULTS: Both ALT and AST activities in serum in LPS group were higher than those in control and berberine treatment group. LPS increased the serum TNF-ɑ content at 2 h after injection, which was reversed by berberine pretreatment. The histological examination showed that LPS caused severe hepatic cell edema, degeneration, apoptosis and even necrosis, and ultrastructure observation demonstrated that LPS induced mitochondrial swelling, condensation and margination of chromatin, irregular nuclear envelope in hepatocytes. The above pathological changes produced by LPS were attenuated by berberine pretreatment. Moreover, MDA contents in liver tissue were higher in LPS group than control and berberine treatment group, but there were no significant difference in SOD activity between berberine treatment and LPS group. CONCLUSION: Berberine has a protective effect on LPS-induced liver injury in mice, the mechanisms may be related to its decreasing the production of TNF-α, inhibiting lipid peroxidation and protecting mitochondria.     

Effect of gingko biloba extract on liver from experimental type 2 diabetic rats

AIM:To study the protective effect of the ginkgo biloba (EGB) extract on liver from experimental type 2 diabetic rats and to explore its possible mechanism. METHODS:Thirty-nine male Sprague-Dawley rats were divided randomly into four groups: normal control group, high-fat group, diabetic group and EGB-treated group. After fed with high-fat diet for 4 weeks, the later two groups were injected with streptozotocin intraperitoneally to induce type 2 diabetes mellitus. EGB-treated group was injected intraperitoneally with EGB at a dose of 8 mg·kg^-1·d^-1, and the other three groups were treated with normal saline of the same volume. After 8 weeks, the morphologic change of hepatic tissue was observed under transmission electron microscope (TEM) and light microscope (LM), respectively. In addition, the activity of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-PX), total nitric oxide synthase (TNOS), inducable nitric oxide synthase (iNOS) and the content of malondialdehyde (MDA), nitric oxide (NO) in liver homogenate were detected biochemically. RESULTS:Obvious liver fatty degeneration, apparent decrease of glycogen granules in cytoplasm of hepatocytes under light microscope and hepatocytes pyknosis, lots of lipid deposits in cytoplasm of hepatocytes, proliferation of hepatic stellate cells and collagen under TEM were observed in diabetic group. The activity of SOD, CAT, GSH-PX decreased but the activity of tNOS, iNOS and the content of MDA, NO^-₂/NO^-₃ increased in diabetic group compared with normal control group. The pathological change was relieved in EGB-treated group. The activity of SOD, CAT, GSH-PX increased, the activity of tNOS, iNOS and the content of MDA, NO^-₂/NO^-₃ decreased in the liver of rats in EGB-treated group compared with diabetic group. CONCLUSION:EGB exerts a beneficial effect on liver in experimental type 2 diabetic rats. Anti-lipid peroxidation and suppression of NO production may be involved in this process.     

The influence of seawater on lipid peroxidation of the muscle tissue wounded by firearm in rabbit limbs

AIM: The influence of the seawater on the lipid peroxidation of the muscle tissue wounded by firearm was studied. METHODS: Both two limbs of rabbits were wounded by the steel ball of 250 mg. The wounded rabbits were divided into two group: One is seawater immersed group (SIG), which was dipped in artificial seawater for 30 min. Another is the single wounded group (SWG), which wasn't dipped in seawater. Then, muscle tissues 0.5 cm (A area), 1.5 cm (B area) and 2.5 cm (C area) from wound edge were cut for biochemical analysis at 3, 6, 12, 24 h of post-wound, respectively. The contents of ATP, MDA and SOD activity of all these tissues were detected, pre-wounded muscle tissues were used as control group. RESULTS: The content of MDA in SIG increased obviously at 3, 6 h, respectively, but it decreased slightly at 12 h and increased again at 24 h. The change in MDA in SWG is similar to that in SIG but more slightly. The changes in both the activity of SOD and the content of ATP in two groups is similar to that of MDA. CONCLUSION: Seawater induced more serious lipid peroxidation in the muscle tissue wounded by firearm.     

Lipid peroxidation precedes TNF and PDGF release in alveolar macrophage of the experimental pulmonary fibrosis rats

AIM:To evaluate the role of alveolar macrophage(AM)lipid peroxidation in bleomycin(BLM)-induced TNF-and PDGF release from AM in rats.METHODS:Male SD rats were intratracheal y instilled with saline or BLM(5 mg/kg body weight), and AM were isolated and analyzed for malondialdehyde(MDA)and glutathione peroxidase(GSH-Px)following 1, 3, 7, 14 or 28 day(s).Simultaneously, TNF-and platelet-derived growth factor(PDGF)were also determined in AM-conditoned media by ELISA and bioassay respectively.RESULTS:(1)MDA in AM was markedly increased on day1, peaked on day 3 and then decreased to near control level on day 7;on the other hand, GSH-Px activity in AM were decreased to non-detectable levels during day 1-7 after BLM instillat ion, returned to the control level by day 14.(2)TNF-and PDGF were increased significantly from the third day on and then exhibited a consectutive changes.(3)AM lipid peroxidation preceded TNF-and PDGF release.CONCLUSION:Prior oxidative changes leading to AM lipid peroxidation, depletion of antioxidative pool might be essential for the subsequent mediators release in BLM-induced pulmonary fibrosis.     

Oxidative stress-activated JNK-MAPK signaling pathway is involved in fluctuant high glucose-induced injury of hepatocytes

AIM: To explore the mechanisms of fluctuant high blood glucose-induced apoptosis of hepatocytes. METHODS: SD rats were randomly divided into normal control group (N), stable high blood glucose group (S), fluctuant high blood glucose group (F) and insulin group (I). Diabetic rats were induced by intraperitoneal injection of streptozotocin (65 mg/kg), and the fluctuant high blood glucose animal model was induced by intraperitoneal injection of ordinary insulin and glucose at different time points every day. The blood glucose fluctuation patterns of the animals in F group within 12 weeks were similar every day and no significant difference of the HbA1c concentration was observed compared with S group, indicating that the fluctuant hyperglycemia was successfully established in F group. The activity of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), and the content of malondialdehyde (MDA) and nitric oxide (NO) in the homogenate of the liver tissues were detected by colorimetry. The mRNA and protein levels of JNK, p-JNK, Bax and Bcl-2 were examined by RT-PCR and Western blot. RESULTS: After 12 weeks, the increases in the intakes of food and water, the urine output, and the abnormal liver function were observed in S group, I group and F group. Compared with N group, the MDA level was increased, the content of NO and the activity of SOD and GSH-Px were decreased, and up-regulation of JNK mRNA and p-JNK and Bax proteins, and down-regulation of Bcl-2 were also found in S group, I group and F group. The above effects were more obviously showed in F group. CONCLUSION: Oxidative stress activates JNK-MAPK signaling pathway, which is involved in fluctuant high glucose-induced apoptosis of hepatocytes.     

Apoptosis in rat hepatocytes with ischemia/reperfusion injury

AIM: To investigate the distributive rules of apoptosis index (AI) in liver with ischemia/reperfusion (I/R) injury and evaluate the factors related to the hepatocyte apoptosis. METHODS: Sixty SD rats in specific pathogen free grade were randomly divided into three groups: control group (n=18), sham operation group (n=18) and I/R group (n=24). In I/R group, liver injury was induced by blocking blood inflow in rat liver for 20 min, then reperfusion for 22 h. Rats in the control group didnt receive any management. Rats in the sham operation group only subjected sham operation. All rat blood samples and livers were obtained for determination. Blood serum ALT, AST, TBIL, TNF-α, IFN-γ, IL-4, plasma endotoxin concentration, MDA level and SOD activity in liver were detected. Hepatic histological analysis was conduced through HE staining. Apoptosis was detected by TUNEL methods. RESULTS: Focal necrosis occurred in six rats livers in I/R group, in control group and sham group no necrosis cell was found in livers. The hepatic AI of I/R group was significantly increased compared with other groups. The AI in region under hepatic amicula was higher than that in central veins region and portal area. The necrotic regions contained apoptotic cells and AI was higher than that of other regions. Hepatic AI was significantly associated with ALT, AST, TNF-α, IFN-γ and SOD/MDA. CONCLUSION: In liver with I/R injury, the apoptotic cells in the region under hepatic amicula and the focus of necrosis are significantly higher than those in other regions, apoptotic cells and necrosis cells co-exist in the same zone. Hepatic AI may be significantly associated with ALT, AST, TNF-α and SOD/MDA.     

柑橘日灼病果皮抗氧化代谢的变化

 以砂糖橘、贡柑、红江橙和暗柳橙为试材,调查其田间日灼率和果实日灼后果皮抗氧化水平的变化。结果表明,不同品种田间日灼率不同;果实发生日灼后果皮组织中超氧阴离子自由基大量积累,脂氧合酶（LOX）活性显著增强,脂质过氧化产物丙二醛（MDA）含量显著上升,加剧细胞膜脂过氧化。超氧化物歧化酶（SOD）活性、抗坏血酸（AsA）和谷胱甘肽（GSH）含量均显著下降,过氧化物酶（POD）和多酚氧化酶（PPO）活性均显著增强,说明其抗氧化代谢失调。     

Dexmedetomidine attenuates acute alcoholic hepatic injury in mice

AIM: To investigate the effects of dexmedetomidine (DEX) on acute alcoholic hepatic injury in mice and to explore the possible mechanisms. METHODS: Kunming mice (n=50) were randomly divided into 5 groups (n=10): normal saline control (NS) group, acute alcoholic hepatic injury model (E) group, low-dose (10 μg/kg) DEX (E+L) group, medium-dose (50 μg/kg) DEX (E+M) group and high-dose (100 μg/kg) DEX (E+H) group. The animals were sacrificed at 6 h after gavage of alcohol or normal saline. The levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), triglyceride (TG), malondialdehyde (MDA), glutathione (GSH) and superoxide dismutase (SOD) were measured. The livers were removed for evaluation of histological characteristics and determining the content of tumor necrosis factor-α (TNF-α) amd interleukin-1β (IL-1β) in the liver tissues by ELISA. The expression levels of cytochrome P450 2E1 (CYP2E1) and nuclear factor-κB (NF-κB) in the liver tissues were evaluated by Western blot. RESULTS: Compared with NS group, the levels of ALT, AST and TG were obviously increased in E group, which were obviously decreased in E+M and E+H groups. Compared with NS group, the levels of TNF-α, IL-1β and MDA were obviously increase in E group, which were obviously decreased in E+M and E+H groups. Compared with NS group, the activity of SOD and the content of GSH were obviously decreased in E group, which were obviously increased in E+M and E+H groups. Compared with NS group, the expression of CYP2E1 and NF-κB was obviously increase in E group, which was obviously decreased in E+M and E+H groups. Compared with NS group, ethanol induced marked liver histological injury, which was less pronounced in E+M and E+H groups. CONCLUSION: DEX has a protective effect on mouse liver with acute alcoholic injury by the involvement in the processes of antioxidation and antiinflammation, and its mechanism may be associated with the inhibition of CYP2E1 and NF-κB expression.     

Oxygen free radical injury of myocardial mitochondria in the experimental type 2 diabetic rats

AIM: To study the mechanism of diabetic cardiomyopathy and abnormality of oxygen free radicals. METHODS: The contents of myocardial cytosolic cytochrome C, mitochondria cytochrome C, mitochondrial calcium, NO, MDA and the activity of SOD and NOS were determined in diabetic rats induced by STZ. The pathological changes were observed under transmission electron microscope. RESULTS: Compared to the normal and ganoderma group, the levels of mitochondrial NO, iNOS, MDA, calcium and plasma Cyt-C in rat myocardium were higher (P<0.05), while mitochondrial Cyt-C and SOD were lowered in model group (P<0.05). The bouncary indistinct, disorganization, a focal loss of muscular fibril, myocardium mitochondria swelling, pulmonary vascular endothelial cellular swelling and obstructed lumen of the capillary were also observed under transmission electronic microscope. CONCLUSION: The findings indicate that oxyradical and lipid peroxidation might be associated with the damage of myocardial mitochondria in NIDDM rats. Cyt-C and mitochondrial calcium is also involved in the process.     

水分亏缺条件下草莓幼苗几个水分生理指标的变化

在离体脱水和不同浓度蔗糖溶液培养条件下,对草莓幼苗的脂质过氧化作用产物丙二醛、过氧化物歧化酶、细胞膜相对透性和组织相对含水量的变化及其相互关系进行研究。结果表明:随着组织相对含水量降低,丙二醛含量增高,细胞膜相对透性增大;丙二醛含量和组织相对含水量之间呈负相关;r新茎=0.89(HS),r叶片=0.75(HS),组织细胞膜相对透性随着丙二醛含量的增高而增大;在离体条件下过氧化物歧化酶对丙二醛含量增高有一定抑制作用。     

Effect of berberine on oxidative damage and the SIRT1/p53 pathway in liver tissues of NAFLD rats

AIM:To investigate the effect of berberine on oxidative damage and silent mating type information regulation 2 homolog 1 (SIRT1)/p53 pathway in the liver tissues of nonalcoholic fatty liver disease (NAFLD) rats and to explore the mechanism of berberine against NAFLD. METHODS:The male SD rats (n=24) were randomly divided into normal group, model group and berberine group (8 rats in each group). The rats in normal group was fed with normal diet, while the rats in model group and berberine group were fed with high-fat diet. The rats in berberine group was intragastrically administered with daily doses (100 mg/kg) of berberine for 16 weeks. The levels of liver total cholesterol (TC), triglyceride (TG), superoxide dismutase (SOD), malondialdehyde (MDA) and total anti-oxidant capatity (T-AOC) were measured. HE staining, oil red O straining and transmission electron microscopy were used to observe the histological changes of the livers. The protein levels of SIRT1, p53 and acetylated p53 (Ac-p53) were determined by Western blot. RESULTS:Compared with model group, the levels of liver TC, TG and MDA in berberine group were significantly reduced (P<0.05 or P<0.01), and the levels of SOD and T-AOC were significantly increased (P<0.01). The results of pathological observation showed that the lipid accumulation in the liver of berberine group was significantly attenuated. Compared with model group, the expression of SIRT1 was significantly increased and the expression of Ac-p53 was obviously reduced in berberine group (P<0.01). CONCLUSION:Berberine reduces hepatic steatosis and oxidative damage in NAFLD rats induce by high-fat diet, and this effect may be associated with regulation of the SIRT1/p53 signal pathway.     

高温处理对温州蜜柑幼果膜脂过氧化作用和乙烯生成的影响

以3年生枳砧兴津温州蜜柑盆栽苗为试材,研究高温处理对柑桔幼果细胞膜脂过氧化作用和内原乙烯水平的影响,及其与幼果脱落的关系,以探讨柑桔高温热害的生理机制.结果表明:高温处理使SOD活性下降,MDA含量增加;膜脂脂肪酸组分中亚麻酸比例减少,硬脂城比例上升;致使股脂不饱和脂肪酸指数下降;加速了内原乙烯合成;加剧了幼果脱落.细胞膜脂脂质过氧化产物MDA含量与不饱和脂肪酸指数呈极显著负相关(r=-0.8407),而与幼果累积落果率呈极显著正相关(r=0.8707).细胞膜脂过氧化作用加剧可能是高温热害加速幼果脱落的初始反应.