著者
Chong-gui Zhu Ya-xin Liu Hao Wang Bao-ping Wang Hui-qi Qu Bao-li Wang Mei Zhu
出版者
The Japan Endocrine Society
雑誌
Endocrine Journal (ISSN:09188959)
巻号頁・発行日
vol.64, no.7, pp.663-673, 2017 (Released:2017-07-28)
参考文献数
35
被引用文献数
35 40

The purpose of this study was to determine whether treatment using the active form of vitamin D (1,25(OH)2D3) could protect against high-fat diet (HFD)-induced non-alcoholic fatty liver disease (NAFLD) in rats and ameliorate oxidative stress. Male Sprague-Dawley rats were divided into three groups and treated with standard chow, HFD, or HFD plus intraperitoneal injection of 1,25(OH)2D3 (5 μg/kg body weight, twice per week), respectively, for 16 weeks. Serum lipid profiles, hepatic function, intrahepatic lipid, and calcium levels were determined. Hepatic histology was examined using hematoxylin/eosin, Masson’s trichrome, and Oil Red O staining. Oxidative stress was assessed by measuring hepatic malondialdehyde (MDA) and F2α-isoprostane content. Expression of nuclear factor-erythroid-2-related factor 2 (Nrf2) and downstream target genes was analyzed using quantitative RT-PCR. 1,25(OH)2D3 treatment improved the serum lipid profile, reduced intrahepatic lipid levels, and attenuated hepatic steatosis and inflammation in HFD rats. Furthermore, MDA and F2α-isoprostane levels in liver tissue were reduced by 1,25(OH)2D3 administration. Although 1,25(OH)2D3 did not regulate the expression of Nrf2 mRNA, it did induce Nrf2 nuclear translocation. The expression of Nrf2 target genes, including Gclc, Nqo1, Sod2, and Cat, was up-regulated by 1,25(OH)2D3. We conclude that 1,25(OH)2D3 protects against HFD-induced NAFLD by attenuating oxidative stress, inducing NRF2 nuclear translocation, and up-regulating the expression of genes encoding antioxidant enzymes.
著者
Jing Xue Xiaorong Li Ping Liu Ke Li Liping Sha Xiaoli Yang Lili Zhu Zhen Wang Youping Dong Li Zhang Hong Lei Xiaoxia Zhang Xiaoying Dong Hao Wang
出版者
The Japan Endocrine Society
雑誌
Endocrine Journal (ISSN:09188959)
巻号頁・発行日
pp.EJ18-0567, (Released:2019-07-03)
被引用文献数
71

Polycystic ovary syndrome (PCOS) represents an endocrine disorder, which is closely related with gut microbiota. Inulin, a kind of probiotics, has been proven to alleviate gut microbiota dysbiosis. Metformin, a biguanide agent, shows beneficial effects on chronic metabolic diseases. Our objective was to assess the effects and associated mechanisms of inulin and metforin on attenuation of PCOS in mice. Mice were divided into 4 groups: control group (CON), model group (MOD), inulin group (INU), metformin group (MET). The last three groups were fed 6 mg of dehydroepiandrosterone (DHEA) per 100 g body weight and 60% high-fat diet to generate mice model. After 21 days of intervention, mice were euthanized and associated indications were investigated. Body weight (BW) and testosterone (T) levels were significantly decreased, but estradiol (E2) levels were increased in INU or MET group, respectively. Ovary HE staining demonstrated that inulin or metformin ameliorated PCOS morphology. Inflammatory indicators from plasma and ovary including TNF-α, IL-6, and IL-17A were decreased in INU or MET group. Moreover, IL-10 in ovary of INU or MET group was increased. Sequencing and analysis of gut microbiota showed that compared to MOD group, Bifidobacterium was increased, but Proteobacteria, Helicobacter and Parasutterella were decreased in INU group. Helicobacter was decreased in MET group. Correlation analysis showed that gut microbiota was correlated with inflammatory factors. Our results revealed that inulin and metformin alleviated PCOS via anti-inflammation and modulating gut microbiota, which may contribute to potential clinical therapy for the disease.
著者
Xiaochen Liu Wenxiao Jia Hong Wang Yunling Wang Jingxun Ma Hao Wang Xuan Zhou Guohua Li
出版者
National Institute of Infectious Diseases, Japanese Journal of Infectious Diseases Editorial Committee
雑誌
Japanese Journal of Infectious Diseases (ISSN:13446304)
巻号頁・発行日
vol.68, no.2, pp.89-97, 2015 (Released:2015-03-23)
参考文献数
34
被引用文献数
4 8

This study aimed to establish a spinal tuberculosis model by implanting Mycobacterium tuberculosis strain H37Rv into the lumbar vertebral body of New Zealand white rabbits. A hole was first drilled into the top of the 6th lumbar vertebra of each rabbit, which was then filled with a gelatin sponge to adsorb 0.2 ml of M. tuberculosis suspension (107 CFU /ml) for the infection group or normal saline for the control group. The holes were then closed with sutures. CT findings demonstrated that 5 and 10 rabbits developed spinal tuberculosis at 4 and 8 weeks, respectively, after this procedure. MRI examinations revealed that 7 and 15 rabbits had positive results at 4 and 8 weeks, respectively, after this procedure. HE staining of the vertebral body and paravertebral soft tissue biopsies of infected rabbits indicated inflammatory cell infiltration or necrosis in 15 rabbits. M. tuberculosis was cultured in 67% of the abscesses. The modeling success rate was 68.1%. By implanting an appropriate dosage of M. tuberculosis strain H37Rv into a local lumbar vertebral body of New Zealand white rabbits, we successfully established a spinal tuberculosis model, the pathological changes of which are similar to those of human spinal tuberculosis.