Hongrui Li;Xianyun Wang;Xiaoying Li;Xueyang Zhou;Xuan Wang;Tiantian Li;Rong Xiao;Yuandi Xi
Nutrition Research and Practice
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v.17
no.2
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pp.371-385
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2023
BACKGROUND/OBJECTIVES: Soy isoflavone (SIF) and soy lecithin (SL) have beneficial effects on many chronic diseases, including neurodegenerative diseases. Regretfully, there is little evidence to show the combined effects of these soy extractives on the impairment of cognition and abnormal cerebral blood flow (CBF). This study examined the optimal combination dose of SIF + SL to provide evidence for improving CBF and protecting cerebrovascular endothelial cells. MATERIALS/METHODS: In vivo study, SIF50 + SL40, SIF50 + SL80 and SIF50 + SL160 groups were obtained. Morris water maze, laser speckle contrast imaging (LSCI), and hematoxylin-eosin staining were used to detect learning and memory impairment, CBF, and damage to the cerebrovascular tissue in rat. The 8-hydroxy-2'-deoxyguanosine (8-OHdG) and the oxidized glutathione (GSSG) were detected. The anti-oxidative damage index of superoxide dismutase (SOD) and glutathione (GSH) in the serum of an animal model was also tested. In vitro study, an immortalized mouse brain endothelial cell line (bEND.3 cells) was used to confirm the cerebrovascular endothelial cell protection of SIF + SL. In this study, 50 µM of Gen were used, while the 25, 50, or 100 µM of SL for different incubation times were selected first. The intracellular levels of 8-OHdG, SOD, GSH, and GSSG were also detected in the cells. RESULTS: In vivo study, SIF + SL could increase the target crossing times significantly and shorten the total swimming distance of rats. The CBF in the rats of the SIF50 + SL40 group and SIF50 + SL160 group was enhanced. Pathological changes, such as attenuation of the endothelium in cerebral vessels were much less in the SIF50 + SL40 group and SIF50 + SL160 group. The 8-OHdG was reduced in the SIF50 + SL40 group. The GSSG showed a significant decrease in all SIF + SL pretreatment groups, but the GSH showed an opposite result. SOD was upregulated by SIF + SL pretreatment. Different combinations of Genistein (Gen)+SL, the secondary proof of health benefits found in vivo study, showed they have effective anti-oxidation and less side reaction on protecting cerebrovascular endothelial cell. SIF50 + SL40 in rats experiment and Gen50 + SL25 in cell test were the optimum joint doses on alleviating cognitive impairment and regulating CBF through protecting cerebrovascular tissue by its antioxidant activity. CONCLUSIONS: SIF+SL could significantly prevent cognitive defect induced by β-Amyloid through regulating CBF. This kind of effect might be attributed to its antioxidant activity on protecting cerebral vessels.
Journal of the Korean Society of Food Science and Nutrition
/
v.30
no.1
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pp.119-126
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2001
Effects of Sardine Oil Feeding and Vitamin E Supplementation on Histopathological Changes and $\alpha$-L-fucosidase activity in experimental hepatocarcinogenesis. Sprague-Dawley rats weighing 80~90 g were fed the diet containing either 15% corn oil (CO) or sardine oil (SO) with or without vitamin E supplements (dl-$\alpha$-tocopherol acetate 800 IU/kg diet) for 8 weeks. After 2 weeks of feeding, the rats were given a single intraperitoneal injectin of diethylnitrosamine (DEN, 200 mg/kg BW). From the fifth week, rats were given 0.02% acetylaminofluorene (AAF) in diet for 4 weeks. At the seventh week, 0.05% phenobarbital in liver and hepatic glutathione S-transferase palcental form positive (GST-P+) foci were examined by Hematoxylin& Eosin (H&E) staining and immunohistochemical method, respectively. Serum $\alpha$-L-fucosidase activity was determined. The livers fromt he carcinogen treated rats showed significantly increased formation of GST-P+ foci at sacrifice points while the livers fromthe non-carcinogen treated groups showed almost no foci. Although GST-P+ foci formation was not affected by dietary oil, it was increased unexpectedly by vitamin E supplementation. Histopathological changes were similar to patterns of GST-P+ foci formation in almost all groups. Serum $\alpha$-L-fucosidase activities were increased by carcinogen treatment in all dietary groups. $\alpha$-L-fucosidase activities were positively correlated with GST-P+ foci formation. There results suggest that excessive vitamin E supplementation can enhance hepatocarcinogenesis although the mechanisms involved are not clearly understood.
Silymarin has been introduced fairly recently as a hepatoprotective agent. But its mechanisms of action still have not been well established. The aim of this study was to make alcoholic fatty liver model of rats in a short time and investigate silymarin's protective effects and possible mechanisms on alcoholic fatty liver for rats. The model of rat's alcoholic fatty liver was induced by intragastric infusion of ethanol and high-fat diet for six weeks. Histopathological changes were assessed by hematoxylin and eosin staining (HE). The activities of alanine transarninase (ALT) and aspartate aminotransferase (AST), the levels of total bilirubin (TBIL), total cholesterol (TC) and triglyceride (TG) in serum were detected with routine laboratory methods using an autoanalyzer. The activities of superoxide dismutase (SOD) and glutathione peroxidase (GPx) and the level of malondialdehyde (MDA) in liver homogenates were measured by spectrophotometry. The TG content in liver tissue was determined by spectrophotometry. The expression of nuclear factor-${\kappa}B$ (NF-${\kappa}B$), intercellular adhesion molecule-1 (ICAM-1) and interleukin-6 (IL-6) in the liver were analyzed by immunohistochemistry. Silymarin effectively protected liver from alcohol-induced injury as evidenced by improving histological damage situation, reducing ALT and AST activities and TBIL level in serum, increasing SOD and GPx activities and decreasing MDA content in liver homogenates and reducing TG content in liver tissue. Additionally, silymarin markedly downregulated the expression of NF-${\kappa}B$ p65, ICAM-1 and IL-6 in liver tissue. In conclusion, Silymarin could protect against the liver injury caused by ethanol administration. The effect may be related to alleviating lipid peroxidation and inhibiting the expression of NF-${\kappa}B$.
Objectives This study aims to evaluate the wound healing effects of oral administered hot water extracts of Korean black ginseng (KBG). Methods 40 C57BL/6 mice were divided into five groups; normal, control, vitamin E 200 mg/kg, KBG 100 mg/kg, KBG 200 mg/kg, each n=8. Skin wounds were made in the back of all mice except normal group using biopsy punches. Wounds were observed on days 7 and 14 after injury. The anti-oxidant and inflammatory protein levels were evaluated using western blotting. Skin tissue was analyzed by hematoxylin & eosin and Masson's trichrome staining method. Results KBG significantly accelerated reducing wound area. KBG significantly decreased myeloperoxidase activity. KBG significantly decreased oxidative stress factors such as NADPH oxidase-4 and p22phox and increased antioxidant enzymes including nuclear factor erythroid 2-related factor2, kelch-like ECH-associated protein-1, heme oxygenase-1, superoxide dismutase, catalase and glutathione peroxidase-1/2. Moreover, KBG significantly decreased inflammation factors including nuclear factor-κB, phosphorylated inhibitor of κBα, cyclooxygenase-2, inducible nitric oxide synthase, tumor necrosis factor-α and interleukin (IL)-6 and increased anti-inflammation cytokine such as IL-4 and IL-10. In addition, KBG significantly increased tight junction proteins including claudin-1, claudin-3, claudin-4. In histopathologic, KBG made the epithelium thin and uniform, and accelerated the remodeling of collagen. Conclusions The results suggest that KBG has healing effects on skin wound in mice by anti-inflammatory and antioxidant activity.
Background: The non-saponin fraction (NSF) of Korean Red Ginseng is a powder in which saponin is eliminated from red ginseng concentrate by fractionation. In this study, we examined the effect of NSF on age-associated sarcopenia in old mice. Methods: NSF (50 or 200 mg/kg/day) was administered orally daily to young (3-6-month-old) and old (20-24-month-old) C57BL/6 J mice for 6 weeks. Body weight and grip strength were assessed once a week during the oral administration period. The gastrocnemius and quadriceps muscle were excised, and the muscle fiber size was compared through hematoxylin and eosin staining. In addition, the effect of NSF on sarcopenia and inflammation/oxidative stress-related factors in hindlimb muscles was investigated by western blotting. Flow cytometry analysis was conducted to investigate the effect of NSF on immune homeostasis. Blood samples were collected by cardiac puncture, and the serum levels of insulin-like growth factor 1, pro-inflammatory cytokines, and glutathione were evaluated. Results: NSF significantly alleviated muscle strength, mass, and also fiber size in old mice. Age-associated impairment of immune homeostasis was recovered by NSF through retaining CD11b+F4/80+ macrophages and regulating inflammatory biomarkers. NSF also decreased the age-induced expression of oxidative stress factors. Taken together, NSF showed the effect of improving sarcopenia by inhibiting low-grade chronic inflammatory/oxidative stress factors. Conclusion: NSF exhibited anti-sarcopenia effects by regulating chronic inflammation and oxidative stress in old mice. Thus, we suggest that NSF is a promising restorative agent that can be used to improve sarcopenia in the elderly as well as maintain immune homeostasis.
Ahmed H. Moustafa;Heba F. Pasha;Manar A. Abas;Adel M. Aboregela
Anatomy and Cell Biology
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v.56
no.1
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pp.109-121
/
2023
Thioacetamide (TAA) exposure and hepatitis C virus infection are usually associated with renal dysfunction. Sofosbuvir (SFV) and daclatasvir (DAC) drugs combination has great value in the treatment of hepatitis C. The study aimed to identify the nephrotoxic effects of TAA and to evaluate the ameliorative role of SFV and DAC in this condition. Forty-eight adult male albino rats were divided into eight groups and received saline (control), SFV, DAC, SFV+DAC, TAA, TAA+SFV, TAA+DAC and TAA+SFV+DAC for eight weeks. Kidney and blood samples were retrieved and processed for histological (Hematoxylin and Eosin and Masson's trichrome), immunohistochemical (α-smooth muscle actin), and biochemical analysis (urea, creatinine, total protein, albumin, malondialdehyde, reduced glutathione, superoxide dismutase, and tumor necrosis factor-α). Examination revealed marked destruction of renal tubules on exposure to TAA with either hypertrophy or atrophy of glomeruli, increase in collagen deposition, and wide expression of α-smooth muscle actin. Also, significant disturbance in kidney functions, oxidative stress markers, and tumor necrosis factor-α. Supplementation with either SFV or DAC produced mild improvement in the tissue and laboratory markers. Moreover, the combination of both drugs greatly refined the pathology induced by TAA at the cellular and laboratory levels. However, there are still significant differences when compared to the control. In conclusion, SFV and DAC combination partially but greatly ameliorated the renal damage induced by TAA which might be enhanced with further supplementations to give new hope for those with nephropathy associated with hepatitis.
Rixin Dai;Xiheng Yang;Wujin He;Qiang Su;Xuexin Deng;Juanfen Li
Korean Circulation Journal
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v.53
no.3
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pp.151-167
/
2023
Background and Objectives: Acute myocardial infarction (AMI) often occurs suddenly and leads to fatal consequences. Ferroptosis is closely related to the progression of AMI. However, the specific mechanism of ferroptosis in AMI remains unclear. Methods: We constructed a cell model of AMI using AC16 cells under oxygen and glucose deprivation (OGD) conditions and a mice model of AMI using the left anterior descending (LAD) ligation. The 3-(4, 5-dimethylthiazol-2-yl)-2, 5 diphenyltetrazolium bromide was employed to determine cell viability. The levels of lactate dehydrogenase, creatine kinase, reactive oxygen species (ROS), glutathione (GSH), malondialdehyde (MDA), and iron were measured using corresponding kits. Dual luciferase reporter gene assay, RNA-binding protein immunoprecipitation, and RNA pull-down were performed to validate the correlations among AC005332.7, miR-331-3p, and cyclin D2 (CCND2). Hematoxylin and eosin staining was employed to evaluate myocardial damage. Results: AC005332.7 and CCND2 were lowly expressed, while miR-331-3p was highly expressed in vivo and in vitro models of AMI. AC005332.7 sufficiency reduced ROS, MDA, iron, and ACSL4 while boosting the GSH and GPX4, indicating that AC005332.7 sufficiency impeded ferroptosis to improve cardiomyocyte injury in AMI. Mechanistically, AC005332.7 interacted with miR-331-3p, and miR-331-3p targeted CCND2. Additionally, miR-331-3p overexpression or CCND2 depletion abolished the suppressive impact of AC005332.7 on ferroptosis in OGD-induced AC16 cells. Moreover, AC005332.7 overexpression suppressed ferroptosis in mice models of AMI. Conclusions: AC005332.7 suppressed ferroptosis in OGD-induced AC16 cells and LAD ligation-operated mice through modulating miR-331-3p/CCND2 axis, thereby mitigating the cardiomyocyte injury in AMI, which proposed novel targets for AMI treatment.
The aim of this study was to investigate the hepatoprotecive effect of silk protein hydrolysates (SDH), which was prepared by acid hydrolysis, in rats. SDH itself did not exhibit any cytotoxic effect on hepatic tissues. SDH showed a protective effect on tert-butyl hydroperoxide (t-BHP)-induced hepatotoxicity and liver damage. SDH effectively reduced AST (aspartate aminotransferase) and ALT (alanine aminotransferase), which are biomarkers for liver damage, in a dose-dependent manner. Malondialdehyde (MDA), a lipid peroxidation product, was significantly reduced by SDH. A high dose of SDH (2 g/kg) reduced t-BHP-induced MDA production by 40%. Glutathione (GSH), which is an endogenous antioxidant molecule, was effectively increased by SDH treatment. GSH content was enhanced by around 2.5-fold, compared with t-BHP control, upon SDH (2 g/kg) treatment. Lactate dehydrogenase (LDH), which is an enzyme released by cell cytotoxicity, was greatly increased by t-BHP, but significantly decreased by SDH treatment. Furthermore, hematoxylin and eosin (H&E) staining showed that SDH suppressed t-BHP-induced lesions in liver tissue. Taken together, SDH might be used as a protective agent against liver damage.
Objectives The purpose of this study was to evaluate the effects of Curcumae Longae Rhizoma pharmacopuncture on the monosodium iodoacetate (MIA)-induced osteoarthritis rats. Methods Osteoarthritis was induced by injection of MIA ($50{\mu}L$ with 80 mg/mL) into knee joint cavity of rats. Rats were divided into 6 groups. Normal group was injected by normal saline into knee joint cavity only. Control group was induced for osteoarthritis by MIA and orally administered with distilled water. Normal Saline group was induced for osteoarthritis by MIA and injected with normal saline $100{\mu}L$. Positive comparison group was injected with MIA and orally administered with indomethacin 5 mg/kg. Curcumae Longae Rhizoma pharmacopuncture low concentration (CL) group was induced for osteoarthritis by MIA and injected with Curcumae Longae Rhizoma pharmacopuncture low concentration $100{\mu}L$. Curcumae Longae Rhizoma pharmacopuncture high concentration (CH) group was induced for osteoarthritis by MIA and injected with Curcumae Longae Rhizoma pharmacopuncture high concentration $100{\mu}L$. Curcumae Longae Rhizoma pharmacopuncture was injected at ST35 and EX-LE4 each group (CL, CH). After that, hind paw weight distribution was measured and oxidative stress biomarker in serum, liver function biomarker in serum, western blot analysis were measured. Histological analysis of knee joint tissue was performed by hematoxylin and eosin staining, Safranin-O staining and Masson's trichrome staining. Results Hind paw weight distribution was significantly improved in both group. alanine aminotransferanse and aspartate aminotransferase were decreased significantly in CH group compare with Indomethacin threated group. Antioxidant enzyme glutathione peroxidase, Catalase and heme oxygenase-1 were increased in CH group compare with control group. Inflammatory cytokine cyclooxygenase-2, inducible nitric oxide synthase and interleukin-1 beta were decreased significantly in CH group. Histological analysis result shows that protective effects of joint and cartilage were observed in both CH and CL groups in a concentration-dependent. Conclusions The result suggest that Curcumae Longae Rhizoma pharmacopuncture has anti-oxidation effect, anti-inflammatory effect and also can prevent progression of osteoarthritis and protect joint cartilage.
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