scholarly journals Allicin Attenuates Inflammation and Suppresses HLA-B27 Protein Expression in Ankylosing Spondylitis Mice

2013 ◽  
Vol 2013 ◽  
pp. 1-6 ◽  
Author(s):  
Xin Gu ◽  
Haishan Wu ◽  
Peiliang Fu
Keyword(s):  
Ankylosing Spondylitis ◽  
Mouse Model ◽  
Protein Translation ◽  
Inflammatory Factors ◽  
High Dose ◽  
Hla B27 ◽  
Wild Type ◽  
Model Group ◽  
Rt Pcr ◽  
Protein Expressions

Here we aimed to determine the therapeutic effect of allicin on ankylosing spondylitis (AS) and explore the mechanism(s) of action. AS mouse model was constructed by transferring the HLA-B2704 gene into Kunming mice and verified by RT-PCR and CT imaging. Verified AS mice were randomly divided into model group (n=6) and allicin-treated groups (50, 100, and 200 mg/kg, resp.,n=6, p.o., for 2 months). Wild type mice were used as control (n=6). The levels of AS-related inflammatory factors were measured by ELISA. mRNA and protein expressions of HLA-B27 were checked by RT-PCR and western blotting. As the results, the mouse model of AS was successfully established, and high-dose allicin could markedly alleviate spine inflammatory injury possibly via reducing the secretion of the inflammatory factors (IL-6, IL-8, and TNF-α) sharply in AS mice. Moreover, allicin significantly inhibited HLA-B27 protein translation but failed to suppress HLA-B27 gene transcription in AS mice, indicating a posttranscriptional mechanism of this modulation. In conclusion, allicin has potential to be used for AS treatment as an anti-inflammatory nutraceutical.

scholarly journals Effect of berberine on hyperandrogenemia, ovulation dysfunction and inflammation in a mouse model of polycystic ovary syndrome

2020 ◽  
Vol 19 (9) ◽  
pp. 1963-1968
Author(s):  
Kena Lu ◽  
Hanmei Lin
Keyword(s):  
Polycystic Ovary Syndrome ◽  
Mouse Model ◽  
Polycystic Ovary ◽  
Inflammatory Factors ◽  
Control Group ◽  
High Dose ◽  
Model Group ◽  
Blank Control Group ◽  
Ovary Syndrome ◽  
Stage Of Development

Purpose: To study the effect of berberine (BBR) on hyperandrogenemia (HA), ovulation dysfunction and inflammation in a mouse model of polycystic ovary syndrome (PCOS).Methods: Forty-five female Kunming mice were randomly divided into control group (9 mice), and mice injected with dehydroepiandrosterone (n = 36) for establishment of PCOS model. The PCOS mice were randomly divided into model group, low-dose BBR (0.25 g/kg), medium-dose BBR (0.5 g/kg) and highdose (1.0 g/kg) groups, with 9 mice in each group. Changes in ovarian morphology were monitored, and sex hormone levels i.e. testosterone (T) and luteinizing hormone (LH)), and inflammatory factors were determined.Results: The model group levels of T and LH were significantly higher than those of the blank control group (p < 0.05), but T and LH levels were significantly lower in middle- and high-dose BBR groups than in the model mice. There were marked increases in IL-6 and TNF-α levels in model mice, when compared to blank control mice, but reduced in the mice treated at the 3 doses of BBR, relative to model mice (p < 0.05). In contrast, the number of follicles was higher at each stage of development in mice for each BBR dose than in the model mice, with increase in corpus luteum.Conclusion: Berberine lowers the weight of PCOS mice, mitigates hyperandrogenemia and inflammatory state, and enhances recovery of ovulation. However, there is need for further studies on its clinic applicability. Keywords: Berberine, Polycystic ovary syndrome, Hyperandrogenemia, Ovulation dysfunction, Inflammatory

scholarly journals Effects of Shugan-Jianpi Recipe on the Expression of the p38 MAPK/NF-κB Signaling Pathway in the Hepatocytes of NAFLD Rats

Medicines ◽  
2018 ◽  
Vol 5 (3) ◽  
pp. 106 ◽  
Author(s):  
Yuanjun Deng ◽  
Kairui Tang ◽  
Runsen Chen ◽  
Yajie Liu ◽  
Huan Nie ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
P38 Mapk ◽  
Low Dose ◽  
Serum Levels ◽  
Inflammatory Factors ◽  
Enzyme Linked Immunosorbent Assay ◽  
High Dose ◽  
Model Group ◽  
Necrosis Factor Alpha ◽  
Tnf Α

Background: In traditional Chinese medicine, the Shugan-Jianpi recipe is often used in the treatment of nonalcoholic fatty liver disease (NAFLD). This study aimed to explore the mechanism of the Shugan-Jianpi recipe in relation to rats with NAFLD induced by a high-fat diet. Methods: Rats were randomly divided into eight groups: normal group (NG), model group (MG), low-dose Chaihu–Shugan–San group (L-CG), high-dose Chaihu–Shugan–San group (H-CG), low-dose Shenling–Baizhu–San group (L-SG), high-dose Shenling–Baizhu–San group (H-SG), low dose of integrated-recipes group (L-IG), and high dose of integrated-recipes group (H-IG). After 26 weeks, a lipid profile, aspartate, and alanine aminotransferases in serum were detected. The serum levels of inflammatory factors including interleukin (IL)-1β, IL-6, and tumor necrosis factor-alpha (TNF-α) were analyzed using the enzyme linked immunosorbent assay (ELISA) method. Hepatic pathological changes were observed with hematoxylin-eosin (HE) and oil red O staining. The expression of the p38 mitogen-activated protein kinases (MAPK)/nuclear factor-κB (NF-κB) pathway was detected by quantitative real-time PCR and Western blotting. Results: A pathological section revealed that NAFLD rats have been successfully reproduced. Compared with the model group, each treatment group had different degrees of improvement. The Shugan-Jianpi recipe can inhibit the serum levels of IL-1β, IL-6, and TNF-α in NAFLD rats. The expression of mRNA and a protein related to the p38 MAPK/NF-κB signaling pathway were markedly decreased as a result of the Shugan-Jianpi recipe. Conclusions: The Shugan-Jianpi recipe could attenuate NAFLD progression, and its mechanism may be related to the suppression of the p38 MAPK/NF-κB signaling pathway in hepatocytes.

scholarly journals Effects of Chaihu-Shugan-San and Shen-Ling-Bai-Zhu-San on p38 MAPK Pathway in Kupffer Cells of Nonalcoholic Steatohepatitis

2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
Qin-He Yang ◽  
Yong-Jian Xu ◽  
Yi-Zhen Liu ◽  
Yin-Ji Liang ◽  
Gao-Fei Feng ◽  
...  
Keyword(s):  
P38 Mapk ◽  
Kupffer Cells ◽  
Mapk Pathway ◽  
Inflammatory Factors ◽  
High Dose ◽  
Model Group ◽  
Expression Levels ◽  
Treatment Groups ◽  
P38 Mapk Pathway ◽  
All Treatment

This study aimed to investigate the effects of Chaihu-Shugan-San (CSS), Shen-Ling-Bai-Zhu-San (SLBZS), and integrated recipe of the above two recipes on inflammatory markers and proteins involved in p38 MAPK pathway in Kupffer cells of NASH rats induced by high fat diet (HFD). Rats were administered at low or high dose of CSS, SLBZS, and integrated recipe except normal group and model group for 16 weeks. The levels of hepatic lipid, TNF-α, IL-1, and IL-6 in liver tissues were measured. Kupffer cells were isolated from livers to evaluate expressions of TLR4, p-p38 MAPK, and p38 MAPK by Western blotting. The results showed that the NASH model rats successfully reproduced typical pathogenetic and histopathological features. Levels of hepatic lipid and liver tissues inflammatory factors in high-dose SLBZS group and integrated recipe group were all lower than that of model group decreased observably. Expressions of TLR4, p-p38 MAPK, and p38 MAPK in Kupffer cells were decreased in all treatment groups, but there was no significant difference between treatment groups. The high-dose SLBZS group had the lowest expression levels of TLR4, and the most visible downtrend in the expression levels of p-p38 MAPK and p38 MAPK was found in the high-dose integrated recipe group. The ratio of p-p38 MAPK to total p38 MAPK protein was obviously increased in all treatment groups. Therefore, our study showed that the activation of p38 MAPK pathway in Kupffer cells might be related to the release of inflammatory factors such as TNF-α, IL-1, and IL-6 in NASH rats. High dose of SLBZS and integrated recipe might work as a significant anti-inflammatory effect in Kupffer cells of NASH rats induced by HFD through suppression of p38 MAPK pathway. It indicated that p38 MAPK pathway may be the possible effective target for the recipes.

scholarly journals Convergent evolution of diverse Bacillus anthracis outbreak strains toward altered surface oligosaccharides that modulate anthrax pathogenesis

PLoS Biology ◽  
2020 ◽  
Vol 18 (12) ◽  
pp. e3001052
Author(s):  
Michael H. Norris ◽  
Alexander Kirpich ◽  
Andrew P. Bluhm ◽  
Diansy Zincke ◽  
Ted Hadfield ◽  
...  
Keyword(s):  
Mouse Model ◽  
Bacillus Anthracis ◽  
Galleria Mellonella ◽  
Death Process ◽  
High Dose ◽  
Wild Type ◽  
Sample Sizes ◽  
Time To Death ◽  
Model Following ◽  
Altered Surface

Bacillus anthracis, a spore-forming gram-positive bacterium, causes anthrax. The external surface of the exosporium is coated with glycosylated proteins. The sugar additions are capped with the unique monosaccharide anthrose. The West African Group (WAG) B. anthracis have mutations rendering them anthrose deficient. Through genome sequencing, we identified 2 different large chromosomal deletions within the anthrose biosynthetic operon of B. anthracis strains from Chile and Poland. In silico analysis identified an anthrose-deficient strain in the anthrax outbreak among European heroin users. Anthrose-deficient strains are no longer restricted to West Africa so the role of anthrose in physiology and pathogenesis was investigated in B. anthracis Sterne. Loss of anthrose delayed spore germination and enhanced sporulation. Spores without anthrose were phagocytized at higher rates than spores with anthrose, indicating that anthrose may serve an antiphagocytic function on the spore surface. The anthrose mutant had half the LD50 and decreased time to death (TTD) of wild type and complement B. anthracis Sterne in the A/J mouse model. Following infection, anthrose mutant bacteria were more abundant in the spleen, indicating enhanced dissemination of Sterne anthrose mutant. At low sample sizes in the A/J mouse model, the mortality of ΔantC-infected mice challenged by intranasal or subcutaneous routes was 20% greater than wild type. Competitive index (CI) studies indicated that spores without anthrose disseminated to organs more extensively than a complemented mutant. Death process modeling using mouse mortality dynamics suggested that larger sample sizes would lead to significantly higher deaths in anthrose-negative infected animals. The model was tested by infecting Galleria mellonella with spores and confirmed the anthrose mutant was significantly more lethal. Vaccination studies in the A/J mouse model showed that the human vaccine protected against high-dose challenges of the nonencapsulated Sterne-based anthrose mutant. This work begins to identify the physiologic and pathogenic consequences of convergent anthrose mutations in B. anthracis.

scholarly journals miR-143-3p impacts on pulmonary inflammatory factors and cell apoptosis in mice with mycoplasmal pneumonia by regulating TLR4/MyD88/NF-κB pathway

2020 ◽  
Vol 40 (7) ◽  
Author(s):  
Yongjun Wang ◽  
Huan Li ◽  
Yongsheng Shi ◽  
Shuying Wang ◽  
Yan Xu ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Group Treatment ◽  
Cell Apoptosis ◽  
Alveolar Epithelial Cell ◽  
Inflammatory Factors ◽  
Model Group ◽  
Alveolar Epithelial ◽  
Protein Expressions ◽  
Epithelial Cell Apoptosis ◽  
Mycoplasmal Pneumonia

Abstract miR-143-3p is correlated with inflammatory pain responses, such as hsa-miR-143-3p expression reduction in fibromyalgia. The present study aimed to explore the effects of miR-143-3p and Toll-like receptor (TLR) 4/myeloid differentiation factor 88 (MyD88)/NF-κB signaling pathway on pulmonary inflammatory factors levels and alveolar epithelial cell apoptosis in mycoplasmal pneumonia mice. Twenty mice were selected as normal group. The 120 successfully modeled Mycoplasma pneumoniae (MP) infection mice were randomly divided into model group (without any treatment), negative control (NC) group (injected with NC mimic), miR-143-3p mimic group (injected with miR-143-3p mimic), miR-143-3p inhibitor group (injected with miR-143-3p inhibitor), TAK-242 group (treatment with TAK-242), and miR-143-3p inhibitor + TAK-242 group (treatment with miR-143-3p inhibitor + TAK-242). Compared with model group, model mice had up-regulated miR-143-3p expression and decreased MyD88 and p-NF-κB p50 protein expressions (all P&lt;0.05); Model mice treated with miR-143-3p mimic and TAK-242 had reduced interleukin (IL)-2 and tumor necrosis factor (TNF)-α contents and protein expressions of MyD88, p-NF-κB p50, increased IL-10 content, fewer alveolar epithelial cell apoptosis, lower Bax expression and higher Bcl-2 expression (all P&lt;0.05); however, mice with miR-143-3p inhibitor treatment showed opposite trends in terms of above indicators. The exacerbation of mycoplasmal pneumonia caused by miR-143-3p inhibitor was partly improved by miR-143-3p inhibitor + TAK-242 combination treatment (all P&lt;0.05). Therefore, up-regulation of miR-143-3p expression may ameliorate pulmonary inflammatory factors levels and reduce alveolar epithelial cell apoptosis in mycoplasmal pneumonia mice by inhibiting TLR4/MyD88/NF-κB signaling pathway.

scholarly journals Different concentrations of Chinese medicine Xiaoyingdaotan Decoction on Hashimoto’s thyroiditis mouse model

2021 ◽  
Author(s):  
Yingjia Zhou ◽  
Hongmei Shen ◽  
Weibo Wen
Keyword(s):  
Chinese Medicine ◽  
Traditional Chinese Medicine ◽  
Mouse Model ◽  
Normal Distribution ◽  
Hashimoto’S Thyroiditis ◽  
Hashimoto's Thyroiditis ◽  
High Dose ◽  
Model Group ◽  
Notch Protein ◽  
The Difference

Abstract Background Through the detection of Notch/Treg/Th17 pathway related factors, to explore the effect of different concentrations of Chinese medicine Xiaoyingdaotan Decoction on Hashimoto's thyroiditis mouse model. Methods To make the mouse model of Hashimoto's thyroiditis, and to administer the Chinese medicine Xiaoyingdaotan Decoction of different concentrations by gavage. After the treatment, the expression of serum Notch protein and Treg/Th17 cytokine levels in mice were detected. The quantitative data conformed to the normal distribution with t test, and did not conform to the normal distribution with Wilcoxon rank sum test. Results The serum Notch protein expression of mice in the model group was significantly higher than that of the other groups, and the difference was statistically significant (P<0.001). Comparing the high-dose Chinese medicine group with the low-dose Chinese medicine group and the model group, the level of the key activation protein FOX-P3 in serum of Treg cells in mice was significantly increased, and the difference was statistically significant (P<0.05). Compared with the model group, the serum TGF-β levels of each group of traditional Chinese medicine were significantly higher than that of the model group, and the difference was statistically significant (P<0.05). The levels of key activating proteins STAT3, RORγt and IL-22 in serum of Th17 cells in each group of traditional Chinese medicine mice were significantly lower than those in the model group, with statistical differences (P<0.05). Conclusion Different concentrations of Chinese medicine Xiaoyingdaotan Decoction can down-regulate the expression of Notch protein in HT mouse model, and can effectively regulate Treg/Th17 cytokines.

scholarly journals The Protective Effects of Maresin 1 in the OVA-Induced Asthma Mouse Model

2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Guochun Ou ◽  
Qin Liu ◽  
Chengxiu Yu ◽  
Xiaoju Chen ◽  
Wenbo Zhang ◽  
...  
Keyword(s):  
Mouse Model ◽  
Signaling Pathway ◽  
Lung Tissue ◽  
Critical Role ◽  
Inflammatory Factors ◽  
High Dose ◽  
Protective Effects ◽  
Cox 2 ◽  
Maresin 1 ◽  
Asthma Mouse Model

Asthma is a chronic inflammatory disease that cannot be cured. Maresin 1 (MaR1) is a specific lipid synthesized by macrophages that exhibits powerful anti-inflammatory effects in various inflammatory diseases. The goal of this study was to evaluate the effect of MaR1 on allergic asthma using an ovalbumin- (OVA-) induced asthma model. Thirty BALB/c mice were randomly allocated to control, OVA, and MaR1 + OVA groups. Mice were sacrificed 24 hours after the end of the last challenge, and serum, bronchoalveolar lavage fluid (BALF), and lung tissue were collected for further analysis. Western blotting was used to measure the protein level of IκBα, the activation of the NF-κB signaling pathway, and the expression of NF-κB downstream inflammatory cytokines. Quantitative real-time polymerase chain reactions (qRT-PCRs) were used to evaluate the expression levels of COX-2 and ICAM-1 in lung tissues. We found that high doses of MaR1 were most effective in preventing OVA-induced inflammatory cell infiltration and excessive mucus production in lung tissue, reducing the number of inflammatory cells in the BALF and inhibiting the expression of serum or BALF-associated inflammatory factors. Furthermore, high-dose MaR1 treatment markedly suppressed the activation of the NF-κB signaling pathway, the degradation of IκBα, and the expression of inflammatory genes downstream of NF-κB, such as COX-2 and ICAM-1, in the OVA-induced asthma mouse model. Our findings indicate that MaR1 may play a critical role in OVA-induced asthma and may be therapeutically useful for the management of asthma.

scholarly journals Antiangiogenesis Roles of Exosomes with Fei-Liu-Ping Ointment Treatment are Involved in the Lung Carcinoma with the Lewis Xenograft Mouse Model

2020 ◽  
Vol 2020 ◽  
pp. 1-14
Author(s):  
Qi Zheng ◽  
Haolong Liu ◽  
Huiting Fan ◽  
Ying Zhang ◽  
Wei Hou
Keyword(s):  
Mouse Model ◽  
Lung Carcinoma ◽  
Animal Studies ◽  
Xenograft Model ◽  
Inflammatory Factors ◽  
Enzyme Linked Immunosorbent Assay ◽  
Model Group ◽  
Xenograft Mouse Model ◽  
Lung Cancer Patients ◽  
Serum Tumour

Exosomes display efficient biocompatibility and represent valuable vehicles for drug or effective material delivery in a tumour-therapeutic approach. Following treatment with Fei-Liu-Ping (FLP) ointment, a traditional Chinese herbal formula, which is used for treating lung cancer patients, could inhibit lung carcinoma growth in clinical and animal studies. In the present study, the values of VEGF and PDGF, which were closely related to angiogenesis, were estimated in serum and carcinoma tissue exosomes to unveil the FLP effects on angiogenesis. The common inflammatory factors of IL-6, IL-1β, TNF-α, and TGF-β in serum exosomes were also detected with the Lewis xenograft model. Methods. Male C57BL/6 mice were randomly divided into four groups, namely, normal, model, cyclophosphamide (CTX), and FLP treatment groups. Histological structures were observed and imaged by H&E. CD31 expressions in tumour tissues were detected by immunofluorescence (IF) and western blot (WB). VEGF, PDGF, and PDGFR levels in exosomes, serum, tumour, and lung tissues were detected by enzyme-linked immunosorbent assay (ELISA), immunohistochemistry (IHC), and WB, respectively. IL-6, IL-1β, TNF-α, and TGF-β levels in exosomes were measured by multiplex immunoassay panels. Results. The results showed that FLP had tumour growth inhibition rate (39.31%). CD31 protein expression was obviously decreased in tumour tissues of CTX- and FLP-treated MO mice, compared to that of MO mice (P<0.05 or P<0.001). VEGF, PDGF, and PDGFR expression levels with FLP treatment were downregulated in exosomes, serum, tumour, and lung tissues compared to model group (P<0.05 or P<0.01). The expressions of IL-6, IL-1β, and TNF-α were downregulated in exosomes compared to the model group (P<0.05 or P<0.01). Conclusions. This study suggested that FLP had the ability of inhibiting tumourigenesis in a Lewis lung xenograft mouse model, whose therapeutic mechanisms might relate with the downregulation of angiogenesis factor and tumour inflammatory cytokines levels.

Effect of Noni on memory impairment induced by hydrocortisone in mice

2021 ◽  
Author(s):  
RUI ZHANG ◽  
JINLIAN LIU ◽  
XINJUAN HOU ◽  
FAN ZHAO ◽  
CHANDI WANG ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Memory Impairment ◽  
Control Group ◽  
Heme Oxygenase 1 ◽  
High Dose ◽  
Related Factor ◽  
Model Group ◽  
Protection Mechanism ◽  
Protein Expressions ◽  
Biochemical Analyses

Abstract Background Oxidative stress and memory impairment have been implicated, a common functional brain disease. Nuclear factor E2-related factor 2 (Nrf2) is highly induced in oxidative stress, indicating that Nrf2 is an emerging target of memory therapy. This study aimed to investigate the effect of Noni on brain memory impairment induced by hydrocortisone and its protection mechanism in mice. Methods Male Kuming mice were (n = 8/group) given hydrocortisone by gastric gavage for 14 consecutive days to establish the memory impairment model except for those in the control group. At the same day, the corresponding drugs were given by gastric gavage. The changes in ethology were examined. Brains were extracted and subjected to western blot analysis and biochemical analyses to assess the activities of oxidative stress. Results The middle and high-dose Noni groups ameliorated the ethology and the high-dose Noni group increased cerebral protein expressions of Nrf2, kelch-like ECH-associated protein 1 (KEAP1) and heme oxygenase-1 (HO-1), as compared to the model group. The arrangement of CA3 vertebral cells in hippocampus of mice was slightly compact and hyperchromatic and pyknosis were alleviated. Furthermore, the biochemical analyses showed the activities of related enzymes of oxidative stress in high-dose Noni group were increased. Conclusions Noni might be a powerful antioxidant that can protect nerve cell and may possess as a potential benefit for the treatment of memory impairment.

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