This study revealed that COST regulates the expression of related inflammatory factors caused by lipid toxicity through the gut microbiota and SCFAs, and improves the liver lipid metabolism of HFD-induced NAFLD mice, laying a foundation for the development of effective and low toxicity drugs for the treatment of NAFLD.

Zhang, J. Feng, Y. Bai, Q. Che, H. Cao, J. Guo and Z. Su, Food Funct. To request permission to reproduce material from this article, please go to the Copyright Clearance Center request page. If you are an author contributing to an RSC publication, you do not need to request permission provided correct acknowledgement is given.

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Cited by. Download options Please wait Supplementary information ZIP K Supplementary information PDF K. Article type Paper. Moreover, this is feasible due to the difference in the amount of UA taken because the UA suspension is insoluble.

Consequently, there is a possibility that the preparation is not homogeneous, while the niosomes are more evenly dispersed than the suspension. An analysis of the study results confirmed that the levels of SGOT and SGPT parameters in the Nio-UA and Nio-UA-CS groups were lower than in the normal group, although not significantly different.

The lower the level, the healthier the condition of the liver In terms of further research, if experimental subjects are used, it is preferable to complete a sampling to check the levels of SGOT and SGPT before the subjects are treated to ensure that their initial condition is healthy.

It is evident from these observations that the administration of Nio-UA-CS can reduce inflammation, pleomorphism, dysplasia, and enlargement of hepatocyte cell nuclei in mice liver. These results indicate that the administration of chitosan to UA niosomes increases the anti-inflammatory and anticancer activity of UA This finding is consistent with those of previous studies regarding CS modification of liposomes which resulted in increased drug activity of UA liposomes and enhanced antitumor drug efficacy Liver histopathology observations were linear with the results of SGOT and SGPT levels indicating that the optimum repair of liver damage occurred in the Nio-UA-CS group followed by Nio-UA and, finally, UA suspension.

Spleen histopathology was also observed in the course of this study. Conventional nanoparticles are known to be trapped by RES, most of which will migrate to the liver and spleen Liposomes and lipid nanocarriers larger than — nm can be taken up by phagocytes. Monocytes, macrophages and neutrophils are phagocytes.

The majority of these phagocytes reside in the liver and spleen for subsequent elimination The administration of Nio-UA-CS indicates lymphoid tissue activation. Such activation is correlated with an increase in immune system activity 37 which can protect the body from non-self-pathogens or cancer cells by destroying them In a previous study on UA nanoparticles with chitosan coating as folate-targeting, the preparation was shown to enhance tumor inhibition and promote an immune-boosting more effectively than free UA 39 , Cldn4 has been recognised as a protein responsible for cell adhesion, polarity and paracellular permeability Intracelullar redistribution results in the weaking of the tight junction leading to the opening of the cells 41 , On the other hand, it has been reported that Cldn4 is not expressed in normal hepatocytes.

However, its expression is increased due to fibrosis, rather than inflammatory condition, of severe liver injury 44 , which this gene expression correlates with differentiation of progenitor cells into mature hepatocytes.

This study also reported that its expression was not found in cases of hepatocellular carcinoma. In addition, NDEA induction has been reported to increase serum bilirubin levels 45 , and UA effectively reduced them, proving its potential efficacy for liver protection and promoting bile secretion 46 , 47 ; however, this study was limited.

Therefore, evaluating the serum bilirubin levels is vital to provide the information associated with the repair of liver damage and its dysfunctions Chitosan coating on UA niosomes can improve the physical morphology of the liver, resulting in the relative weight of the liver and lung organs which are relatively the same as the normal group and there is no significant difference in the difference in body weight.

Chitosan coating on UA niosomes can increase the effectiveness of UA as a therapy to prevent liver damage in subjects induced by N-Nitrosodiethylamine in terms of histopathological parameters of liver tissue which are relatively more normal than negative controls.

Chitosan coating on UA niosomes can increase the effectiveness of UA as a therapy to prevent liver damage in mice induced by N-Nitrosodiethylamine in terms of decreasing serum levels of SGOT and SGPT.

Preparation of niosomes was conducted using a thin layer hydration method with a formula composition referred to previous studies as shown in Table 3 UA sigma-Aldrich, Tokyo, Japan solution in methanol, span 60 Wako Pure Chemical Industries, Ltd.

The organic solvents were then heated in a rotary vacuum evaporator at a temperature of 60 °C until they had all evaporated and a thin lipid layer was formed.

This layer was hydrated using 2 ml PBS solution pH 7. Sonication was carried out with a water bath sonicator to form niosomes in order to reduce the size of the vesicles. Dissolving chitosan Biotech, Cirebon, Indonesia in 0. The addition was completed by mixing 40 µl of chitosan solution with µl of niosomal samples before vortexing for ten seconds.

Approximately µL niosomes was diluted in 2 mL aqua demineralization with particle size and PDI measurements subsequently being completed by the Dynamic Light Scattering method using Malvern Zetasizer Instruments Malvern Panalytical, UK.

Furthermore, µL niosomes were also taken diluted in 2 mL aqua demineralization ζ-potential measured using the Electrophoresis Light Scattering method with Malvern Zetasizer Instruments Malvern Panalytical, UK.

The evaluation was completed three times for each of the Nio-UA and Nio-UA-CS samples. All methods were performed in accordance with ARRIVE guidelines and relevant regulations Five randomly selected subjects formed the members of each treatment group. The negative control group was treated by means of NDEA i.

injection for four weeks, while PBS pH 7. Subjects were given drugs, including UA suspension in 0. After the final UA preparation had been administered, the subjects were left for seven days before their organs were surgically removed.

The decrease in SGOT and SGPT levels was determined from comparisons between each treatment group and the control group. The SGOT and SGPT levels were determined by enzymatic reaction kinetic method. The reagents used were ready-to-use reagents consisting of AST GOT and ALT GPT reagents The subjects were dissected and their livers immediately removed, rinsed with normal saline, and dry wiped with a tissue or filter paper, before finally being weighed, photographed and morphologically examined.

Changes in lobular architecture, bleeding, neutrophilic infiltration, and dysplastic hepatocytes on histopathological preparations of liver tissue were observed by means of light microscopy 45 , To evaluate the organ weight of the subjects, quantitatively each organ of mice in each group was weighed.

Because overall body weight affects the weight of individual organs, the relative weight of the livers was calculated using the formula 53 :. The calculation results relating to the relative weight of the organs in the treatment group were then compared with those of the normal and negative control groups to determine whether significant differences existed.

The quantitative data represent the average and standard deviation of sample measured in replications. A statistical analysis was performed using the one-way variant analysis ANOVA method followed by a Post Hoc Tukey HSD test.

The animal study procedures were performed in accordance with the ethical clearance issued by The Ethics Commission of Faculty of Veterinary Medicine, Universitas Airlangga Certificate number 2.

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Download references. This study was financially supported by a Preliminary Research on Excellence in Higher Education Institutions Penelitian Dasar Unggulan Perguruan Tinggi, PDUPT through Grant No. Department of Pharmaceutical Sciences, Faculty of Pharmacy, Universitas Airlangga, Surabaya, , Indonesia.

Stem Cell Research and Development Center, Universitas Airlangga, Surabaya, , Indonesia. Master Program of Pharmaceutical Sciences, Faculty of Pharmacy, Universitas Airlangga, Surabaya, , Indonesia. Department of Veterinary Science, Faculty of Veterinary Medicine, Universitas Airlangga, Surabaya, , Indonesia.

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Article type Paper. Submitted 07 Sep Accepted 19 Oct First published 03 Nov Download Citation. Food Funct. Request permissions. Ameliorating the effect and mechanism of chitosan oligosaccharide on nonalcoholic fatty liver disease in mice J. Social activity. Search articles by author Jiahua Zhang.

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