Inhibitory effects of Humulus japonicus extract against hepatic injury in a diabetic rat model.
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ABSTRACT: Supplementary information
The online version contains supplementary material available at 10.1007/s10068-021-00924-w.
SUBMITTER: Kim TW
PROVIDER: S-EPMC8302710 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Japanese hop (Humulus japonicus) is a major cause of weed pollinosis in East Asia. However, supplies of commercial allergen extract from this plant have not met clinical demand. The pollen of common hop (Humulus lupulus), a closely related species, may provide an alternative source if there is strong IgE cross-reactivity between these two species. We aimed to compare the IgE cross-reactivity and allergenicity of common hop and Japanese hop pollen.Cross-reactivity was measured by inhibition ELISA. One- and two-dimensional (2D) gel analyses combined with IgE immunoblotting and mass spectrometry [liquid chromatography coupled to electrospray ionization tandem mass spectrometry (LC-ESI-MS/MS)] were performed to detect IgE-reactive pollen components.Up to 16.7% of IgE reactivity to Japanese hop was inhibited by common hop. A 12-kDa protein component of Japanese hop pollen that showed the most potent IgE reaction was absent from common hop. Six IgE-reactive components from Japanese hop were detected by 2D gel electrophoresis and LC-ESI-MS/MS, but showed low Mascot scores, preventing positive identification.No significant IgE cross-reaction was observed for Japanese and common hop pollen allergens. Development of allergy diagnostic and immunotherapeutic reagents based on Japanese hop pollen are urgently needed.
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Project description:Humulus japonicus (HJ) is a widely used herbal medicine in Asia with anti?oxidative, anti?microbial, and anti?inflammatory effects. We investigated the potential therapeutic effects of HJ in rheumatoid arthritis (RA) using a mouse model of collagen?induced arthritis (CIA) and a lipopolysaccharide?stimulated murine macrophage cell line (RAW 264.7). The CIA mice were administered 300 mg/kg HJ orally starting 3 days prior to second immunization. The clinical and histopathological findings were assessed in the paw of CIA mice. The levels of autoantibodies and inflammatory markers were determined in the plasma and cell culture supernatant, respectively. The expression at mRNA and protein levels was analyzed by reverse transcription quantitative?PCR and western blot analysis, respectively. HJ significantly decreased the gross arthritic scores and paw swelling in CIA mice. Furthermore, synovial inflammation, cartilage destruction, and bone erosion were markedly reduced by HJ. It also decreased the expression of inflammatory enzymes in both the paw of mice and RAW 264.7 cells. Moreover, the expression of genes related to all macrophages and pro?inflammatory M1 macrophage were significantly decreased, whereas the expression of anti?inflammatory M2 macrophage marker was markedly increased in the paw of HJ?treated CIA mice. In addition, HJ suppressed the levels of plasma anti?type II collagen antibody following the decreased expression of T helper type 1 (Th1) and Th2 cell?associated surface markers and cytokines in the paw. HJ also significantly inhibited the expression of IL?6 both in vitro and in vivo, followed by reduced STAT3 phosphorylation and expression in the paw of CIA mice. Finally, the expression of osteoclast?related genes was decreased in the paw of HJ?treated CIA mice. These findings suggest that HJ can play a role in suppressing the development of CIA by overall regulation of articular inflammation. This study should provide new insights into the use of HJ as a therapeutically effective natural product against RA.
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Project description:Aims/introductionTo investigate the protective effect of Polygonatum sibiricum polysaccharide (PSP) on the retina in diabetic rats.Materials and methodsA total of 120 Sprague-Dawley rats were randomly divided into blank control, control model (meaning diabetes mellitus), and diabetes mellitus with PSP intervention of high, medium and low doses groups. The difference of retinal vascularization between groups was evaluated by fluorescein isothiocyanate-dextran perfusion. Terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling staining was used to assess apoptosis in the retinal ganglion cells; reverse transcriptase polymerase chain reaction and western blotting were utilized to evaluate the expression of Bcl2-associated X protein, B-cell lymphoma-2 factor, epidermal growth factor, p38 mitogen-activated protein kinases, transforming growth factor-β and vascular endothelial growth factor at the messenger ribonucleic acid and protein level.ResultsFluorescein isothiocyanate-dextran perfusion showed retinal vascular anomaly in diabetes mellitus rats, but vascular tortuosity and leakage were relatively alleviated after PSP intervention. Terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling staining showed numerous terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling-positive retinal cells in the diabetes mellitus group, which then were reduced by PSP treatment. Reverse transcriptase polymerase chain reaction showed that PSP intervention decreased Bcl2-associated X protein, epidermal growth factor, p38 mitogen-activated protein kinases, vascular endothelial growth factor and transforming growth factor-β messenger ribonucleic acid expression, but increased B-cell lymphoma-2 factor messenger ribonucleic acid expression. Western blot showed that PSP intervention upregulated the expression of B-cell lymphoma-2 factor, and downregulated the expression of Bcl2-associated X protein, epidermal growth factor, p38 mitogen-activated protein kinases, vascular endothelial growth factor and transforming growth factor-β proteins.ConclusionsPolygonatum sibiricum polysaccharide shows a protective effect against diabetes-induced retinal injury in a dose-dependent manner. The mechanism of action deserves further study and exploration.
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Project description:A recent study showed that 54% of type 2 diabetes (T2D) patients have nonalcoholic fatty liver disease, which is a risk factor for aggravation diabetic symptoms. Previous studies suggested components in maple syrup alleviated liver injury and found polyphenols as food components to improve the symptoms and complications of diabetes. Therefore, we hypothesized that a polyphenol fraction in maple syrup improves the symptoms and complications of diabetes. To address the hypothesis, we investigated the effects of a polyphenol-rich maple syrup extract (MSE) on a T2D model mice. KK-Ay mice were fed a normal or 0.1% MSE-supplemented diet for 43 days. The results showed that the levels of serum alanine aminotransferase and aspartate aminotransferase were significantly reduced in mice that ingested MSE. Hepatic genes related to lipogenesis and lipolysis were down- and upregulated, respectively, in mice that ingested MSE. These results suggest that MSE intake alleviates liver injury and suppresses lipid accumulation in the livers of T2D mice.
2020-01-13 | GSE134185 | GEO
Project description:Humulus japonicus is an annual plant belonging to the Cannabacea family, and it has been traditionally used to treat pulmonary tuberculosis, dysentery, chronic colitis, and hypertension. We investigated the active components against Parkinson's disease from H. japonicus fraction (HJF) using high performance liquid chromatography (HPLC) coupled with quadruple-time-of-flight mass spectroscopy (qTOF-MS) and NMR. Fourteen compounds were isolated from HJF, including one new compound, using HPLC-qTOF-MS and NMR. The major compounds of HJF were luteolin-7-O-glucoside and apigenin-7-O-glucoside, and there was approximately 12.57- and 9.68-folds increase in the contents of these flavonoids compared to those of the 70% EtOH extract. Apigenin and luteolin exhibited the strongest inhibitory effects on monoamine oxidase (MAO) B enzyme activity. In animal studies, limb-use behavior was significantly reduced by unilateral 6-OHDA lesion and ipsilateral rotations. These results indicated that oral administration of 300 mg/kg HJF resulted in the improvement of motor asymmetry and motor impairment in unilateral 6-OHDA-lesioned mice. HJF, including active components leads to an improvement of motor behavior in a Parkinson's disease mouse model.
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Project description:BackgroundDiabetes mellitus (DM) is marked by oxidative stress, inflammation, and vascular dysfunction that caused diabetic nephropathy that resulted in end-stage renal disease (ESRD). Vascular dysfunction is characterized by an imbalance in vasoconstrictor and vasodilator agents which underlies the mechanism of vascular injury in DM. Additionally, diminished podocytes correlate with the severity of kidney injury. Podocyturia often precedes proteinuria in several kidney diseases, including diabetic kidney disease. Centella asiatica (CeA) is known as an anti-inflammatory and antioxidant and has neuroprotective effects. This research aimed to investigate the potential effect of CeA to inhibit glomerular injury and vascular remodeling in DM.MethodsThe DM rat model was induced through intraperitoneal injection of streptozotocin 60 mg/kg body weight (BW), and then rats were divided into 1-month DM (DM1, n = 5), 2-month DM (DM2, n = 5), early DM concurrent with CeA treatment for 2 months (DMC2, n = 5), and 1-month DM treated with CeA for 1-month (DM1C1, n = 5). The CeA (400 mg/kg BW) was given daily via oral gavage. The control group (Control, n = 5) was maintained for 2 months. Finally, rats were euthanized and kidneys were harvested to assess vascular remodeling using Sirius Red staining and the mRNA expression of superoxide dismutase, podocytes marker, ACE2, eNOS, and ppET-1 using RT-PCR.ResultsThe DM groups demonstrated significant elevation of glucose level, glomerulosclerosis, and proteinuria. A significant reduction of SOD1 and SOD3 promotes the downregulation of nephrin and upregulation of TRPC6 mRNA expressions in rat glomerular kidney. Besides, this condition enhanced ppET-1 and inhibited eNOS and ACE2 mRNA expressions that lead to the development of vascular remodeling marked by an increase of wall thickness, and lumen wall area ratio (LWAR). Treatment of CeA, especially the DMC2 group, attenuated glomerular injury and showed the reversal of induced conditions.ConclusionsCentella asiatica treatment at the early stage of diabetes mellitus ameliorates glomerulosclerosis and vascular injury via increasing antioxidant enzymes.
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Project description:Activation of hepatic stellate cells (HSCs) plays a crucial role in liver fibrogenesis. armepavine (Arm, C19H23O3N), an active compound from Nelumbo nucifera, has been shown to exert immunosuppressive effects on T lymphocytes and on lupus nephritic mice. The aim of this study was to investigate whether Arm could exert anti-hepatic fibrogenic effects in vitro and in vivo. A cell line of rat HSCs (HSC-T6) was stimulated with tumor necrosis factor-alpha (TNF-alpha) or lipopolysaccharide (LPS) to evaluate the inhibitory effects of Arm. An in vivo therapeutic study was conducted in bile duct-ligated (BDL) rats. BDL rats were given Arm (3 or 10 mg/kg) by gavage twice daily for 3 weeks starting from the onset of BDL. Liver sections were taken for fibrosis scoring, immuno-fluorescence staining and quantitative real-time mRNA measurements. In vitro, Arm (1-10 microM) concentration-dependently attenuated TNF-alpha- and LPS-stimulated alpha-SMA protein expression and AP-1 activation by HSC-T6 cells without adverse cytotoxicity. Arm also suppressed TNF-alpha-induced collagen collagen deposition, NFkappaB activation and MAPK (p38, ERK1/2, and JNK) phosphorylations. In vivo, Arm treatment significantly reduced plasma AST and ALT levels, hepatic alpha-SMA expression and collagen contents, and fibrosis scores of BDL rats as compared with vehicle treatment. Moreover, Arm attenuated the mRNA expression levels of col 1alpha2, TGF-beta1, TIMP-1, ICAM-1, iNOS, and IL-6 genes, but up-regulated metallothionein genes. Our study results showed that Arm exerted both in vitro and in vivo antifibrotic effects in rats, possibly through anti-NF-kappaB activation pathways.
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Project description:BackgroundAdipose and hepatic metabolic dysfunctions are critical comorbidities that also aggravate insulin resistance in obese individuals. Melatonin is a low-cost agent and previous studies suggest that its use may promote metabolic health. However, its effects on some comorbidities associated with obesity are unknown. Herein, we investigated the hypothesis that melatonin supplementation would attenuate adipose-hepatic metabolic dysfunction in high fat diet (HFD)-induced obesity in male Wistar rats.Materials and methodsTwenty-four adult male Wistar rats (n = 6/group) were used: Control group received vehicle (normal saline), obese group received 40% high fat diet, melatonin-treated group received 4 mg/kg of melatonin, and obese plus melatonin group received 40% HFD and melatonin. The treatment lasted for 12 weeks.ResultsHFD caused increased food intake, body weight, insulin level, insulin resistance and plasma and liver lipid but decreased adipose lipid. In addition, HFD also increased plasma, adipose and liver malondialdehyde, IL-6, uric acid and decreased Glucose-6-phosphate dehydrogenase, glutathione, nitric oxide and circulating obestatin concentration. However, these deleterious effects except food intake were attenuated when supplemented with melatonin.ConclusionTaken together, the present results indicate that HFD exposure causes adipose-hepatic metabolic disturbance in obese animals, which are accompanied by oxidative stress and inflammation. In addition, the present results suggest that melatonin supplementation attenuates adipose-hepatic metabolic dysfunction, accompanying obesity by suppression of oxidative stress/inflammation-dependent mechanism and increasing circulating obestatin.
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