Food Bioscience
·
2024
·
IF 4.8
Jing Zhang,Jingyi Yang,Xudong Han,Yuyao Ren,Yan Liu,Bohao Zhao,Xinsheng Wu,Yang Chen
Rabbit meat is recognized for its nutritional benefits and affordability. However, research into the primary factors influencing its flavor, especially among various rabbit breeds, remains insufficient. This study conducted a comprehensive comparison of meat quality, metabolomic, and transcriptomic profiles between the longissimus dorsi muscles of Fujian yellow rabbits (FJY) and New Zealand white rabbits (NZW), which exhibit significant variations in body size and growth rate. A total of 68 samples, with 34 from each breed, were analyzed. Results indicated that FJY rabbits had lower body weights but higher dressing percentages than NZW rabbits. FJY meat was higher brightness (L*) and yellowness (b*), lower redness (a*), along with significantly reduced cooking losses. In terms of proximate composition, FJY meat exhibited higher protein and collagen levels but significantly less fat and moisture than NZW meat. Additionally, FJY meat contained higher levels of myristic acid, palmitoleic acid, cis-11-eicosapentaenoic acid, α-linolenic acid, and a higher MUFA/FA ratio. Metabolomic analysis using HPLC-MS/MS identified 231 differential metabolites, including amino acids and their derivatives, organic acids, and heterocyclic compounds. Transcriptomic analysis via RNA-seq revealed 211 differentially expressed genes potentially involved in meat quality regulation. Integrated analyses identified 70 KEGG pathways associated with pivotal genes, such as CPT2, PAK1, SLC7A7, and TAS1R2 , which exhibited correlations with differential metabolites like cholesterol, benzoic acid, putrescine, and N-acetylcysteine, suggesting a synergistic effect on meat quality. Overall, these findings provide valuable insights into the distinct meat quality characteristics that underpin the improved quality and flavor of rabbit meat.
研究领域:
动物科学
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分子生物学
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食品科学
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营养学
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DOI
高影响因子
JOURNAL OF APPLIED TOXICOLOGY
·
2020
·Vol. 40
·期 11
·1491-1497
·
IF 2.997
Youyou Zhang,Liang Liu,Liang Ren
The cardiotoxicity of cantharidin has been well characterized, but the understanding of the underlying mechanism(s) is incomplete. To more fully understand the differentially expressed genes (DEGs) in cantharidin-induced myocardial injury, Sprague-Dawley rats were exposed to cantharidin (1.34 mg/kg or 2.67 mg/kg) for 24 h and then the heart was sampled for pathologic changes analysis and RNA-sequencing-based transcriptomic profiling. In addition, serum troponin T (TN-T) levels were also tested using the enzyme-linked immunosorbent assay method. The results showed that cantharidin could cause myocardial damage and elevated serum TN-T levels. The genes with a fold change ≥2 were considered as DEGs and we found 38 DEGs that were mainly enriched in eight pathways revealed by Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis. The cellular component of gene ontology analysis showed that the DEGs were mostly enriched in the extracellular matrix. In conclusion, our present study demonstrated that cantharidin induces myocardial injury by multiple modulatory mechanisms, which provide new insights for further study of the pathophysiologic mechanism of cantharidin-induced myocardial injury.
研究领域:
药理学
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分子生物学
·
毒理学
·
心脏病学
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产品关联
DOI
PubMed
高影响因子
JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY
·
2020
·
IF 4.192
Jiamu Kang,Liu Liu,Yongfeng Liu,Xiaoyu Wang
Antibiotic resistance and capacity for biofilm formation of Shigella flexneri render previous prevention and control strategies minimally effective. Ferulic acid (FA) has been demonstrated to be useful due to its application in foods as an alternative natural preservative. However, information regarding the S. flexneri phenotype and molecular responses to FA exposure is limited. The present study investigated the effects of FA on S. flexneri planktonic growth and biofilm formation. The results demonstrated that the cell membrane of S. flexneri in planktonic growth mode exhibited irreversible destruction after FA exposure, as characterized by decreased cell viability, leakage of cytoplasmic constituents, accelerated adenosine triphosphate (ATP) consumption, cell membrane depolarization, and cellular morphological changes. FA significantly inhibited S. flexneri adhesion and biofilm formation at a working concentration (1/8 MIC) that almost did not inhibit planktonic growth. Transcriptomics profiling showed that the exposure to a subinhibitory concentration of FA dramatically altered gene expression in the S. flexneri biofilm, as a total of 169 differentially expressed genes (DEGs) were upregulated and 533 DEGs were downregulated, compared to the intact biofilm. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis showed that the DEGs were mainly involved in pathways of ribosomes, ABC transporters, and the citrate cycle. Furthermore, we show that FA altered the transcription of S. flexneri genes associated with adhesion, transcriptional regulation, and the synthesis and transport of extracellular polymeric substances that contribute to biofilm formation. These data provide novel insights into S. flexneri behavioral responses to FA exposure and suggest that FA could effectively constrain S. flexneri and its biofilm formation.
研究领域:
微生物学
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分子生物学
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食品科学
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药理学
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产品关联
DOI
PubMed
高影响因子
AQUATIC TOXICOLOGY
·
2016
·
IF 3.557
Jieyi Li,Jinfeng Liu,Yuhuan Zhang,Xuedong Wang,Weijun Li,Hongqin Zhang,Huili Wang
The toxicity of β-diketone antibiotics (DKAs) to larval and adult zebrafish ( Danio rerio ) was investigated by miRNA sequencing and bioinformatics analyses. In control and DKA-exposed groups, 215 differentially expressed miRNAs were screened, and 4076 differential target genes were predicted. Among 51 co-differentially expressed genes, 45 were annotated in KOG functional classification, and 34 in KEGG pathway analysis. The homology analysis of 20 miRNAs with human hsa-miRNAs demonstrated 17 high homologous sequences. The expression levels of 12 miRNAs by qRT-PCR were consistent with those by sRNA-seq. A regulatory network for 4 positive miRNA genes (dre-miR-10, ⿿96, ⿿92 and ⿿184) was plotted, and the high-degree of connectivity between miRNA-gene pairs suggests that these miRNAs play critical roles during zebrafish development. The consistent expression of dre-miR-184 and dre-miR-96 was proved in 120-hpf zebrafish brain, gill, otoliths and lateral line neuromast by qRT-PCR, miRNA-seq, W-ISH and ISH. DKA-exposure led to vacuolation of interstitial cells, reduced number of neurons, glial cell proliferation and formation of glial scar, and the obvious abnormality of cell structure might result from abnormal expression of differentially expressed miRNAs. In general, chronic DKA-exposure resulted in comprehensively toxic effects on larval and adult zebrafish tissues, especially for nervous system.
研究领域:
水生毒理学
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分子生物学
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生物信息学
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产品关联
DOI
PubMed
高影响因子
JOURNAL OF HAZARDOUS MATERIALS
·
2024
·
IF 12.2
Jinzhi Ren,Ying Peng,Luhang She,Lu Yan,Jianjun Li,Caixia Gao,Chao Wang,Yimeng Wang,Xiangping Nie,Xiaowei Zhang
The estuarine ecological environment faces significant threats from contaminants of emerging concern (CECs); yet, the risk posed by CECs to resident organisms remains poorly understood. Here, we employed tiered toxicity testing to investigate the adverse effects and potential mechanisms of tris (1-chloro-2-propyl) phosphate (TCPP) on the early life stages of an estuarine fish, Mugilogobius chulae . TCPP affected the development of M. chulae embryos, including survival, morphology, hatching, and behavior. A concentration-dependent transcriptomic analysis showed that TCPP disrupted 12 neurodevelopment-related KEGG pathways in M. chulae embryos, with five of the 30 % top-ranked pathways related to neurotransmitter signaling. Besides the cholinergic synapse signaling pathway, the glutamatergic signaling pathway (including NMDAR and AMPAR subtypes) may also mediate TCPP-induced neurodevelopmental toxicity. The NMDAR subtype GRIN2B was downregulated at high concentrations. Molecular dynamics simulations revealed a strong interaction between TCPP and GRIN2B, with TCPP binding to the residues Ile153 and Ile188. The results suggest that NMDARs play a crucial role in TCPP-induced neurodevelopmental toxicity toward M. chulae. AOP network analysis predicted that TCPP may impact cognitive functions and memory. Our study provides a novel testing strategy for identifying the mechanisms of toxicity of CECs, a crucial component of ecological risk assessment.
研究领域:
环境毒理学
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水生生态学
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分子生物学
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神经科学
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产品关联
DOI
PubMed
高影响因子
JOURNAL OF APPLIED TOXICOLOGY
·
2024
·
IF 2.7
Canyang Wang,Zhengzheng Zhou,Yayu He,Juan Li,Yi Cao
Food contaminates, such as insecticide, may influence the toxicity of nanoparticles (NPs) to intestine. The present study investigated the combined toxicity of TiO 2 NPs and fipronil to male mouse intestine. Juvenile mice (8 weeks) were orally exposed to 5.74 mg/kg TiO 2 NPs, 2.5 mg/kg fipronil, or both, once a day, for 5 days. We found that both TiO 2 NPs and fipronil induced some pathological changes in intestines, accompanying with defective autophagy, but these effects were not obviously enhanced after TiO 2 NP and fipronil co-exposure. Fipronil promoted Ti accumulation but induced minimal impact on other trace elements in TiO 2 NP-exposed intestines. Metabolomics data revealed that the exposure altered metabolite profiles in mouse intestines, and two KEGG pathways, namely, ascorbate and aldarate metabolism (mmu00053) and glutathione metabolism (mmu00480), were only statistically significantly changed after TiO 2 NP and fipronil co-exposure. Five metabolites, including 2-deoxy-D-erythro-pentofuranose 5-phosphate, 5alpha-cholestanol, beta-D-glucopyranuronic acid, elaidic acid, and isopentadecanoic acid, and maltotriose, were more significantly up-regulated after the co-exposure, whereas trisaccharide and xylonolactone were only significantly down-regulated by the co-exposure. We concluded that fipronil had minimal impact to enhance the toxicity of TiO 2 NPs to mouse intestines but altered metabolite profiles.
研究领域:
毒理学
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代谢组学
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环境科学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
Frontiers in Pharmacology
·
2021
·
IF 5.811
Yang Bing,Yang Nan,Chen Yaping,Zhu Maomao,Lian Yuanpei,Xiong Zhiwei,Wang Bei,Feng Liang,Jia Xiaobin
Lung cancer is one of the most devastating diseases worldwide, with high incidence and mortality worldwide, and the anticancer potential of traditional Chinese medicine (TCM) has been gradually recognized by the scientific community. Astragali Radix (AR) is commonly used in traditional Chinese medicine in the treatment of lung cancer and has a certain clinical effect, but effective components and targets are still unclear. In the study, we established an integrated strategy for effective-component discovery of AR in the treatment of lung cancer based on a variety of techniques. First, the effective components and potential targets of AR were deciphered by the “component-target-disease” network using network pharmacology, and potential signal pathways on lung cancer were predicted by Gene Ontology (GO) biological function enrichment analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses. Then, the therapeutic effects of AR in the treatment of lung cancer were evaluated in vivo using A/J mice, and the potential targets related to autophagy and potential signal pathway were verified by Western blot analysis, immunofluorescence staining, and real-time PCR technology at protein and gene expression level. Finally, metabolism in vitro by rat intestinal flora and cell membrane immobilized chromatography technology were used to screen the effective components of AR in the treatment of lung cancer, and remaining components from the cell immobilized chromatography were collected and analyzed by ultra-performance liquid chromatography–electrospray quadrupole time-of-flight mass spectrometry (UPLC-Q-TOF-MS). The screening results of the integrated strategy showed that calycosin-7-O-β-D-glucoside, ononin, calycosin, astragaloside IV, astragaloside II, cycloastragenol, and formononetin may be effective components of AR in the treatment of lung cancer, and they may play a role in the treatment of lung cancer through autophagy and p53/AMPK/mTOR signaling pathway. The integrated strategy for effective-component discovery provided a valuable reference mode for finding the pharmacodynamic material basis of complex TCM systems. In addition, the prediction for targets and signal pathways laid a foundation for further study on the mechanism of AR in the treatment of lung cancer.
研究领域:
药理学
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肿瘤学
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中医药
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分子生物学
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生物信息学
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产品关联
DOI
PubMed
高影响因子
JOURNAL OF APPLIED TOXICOLOGY
·
2020
·Vol. 41
·期 8
·1275-1285
·
IF 2.997
Shan Yi,Yan-ping Liu,Xun-ya Li,Xiao-yan Yuan,Ye Wang,Ying Cai,Yuan-di Lei,Lian Huang,Zhao-hui Zhang
Beryllium and its compounds are systemic toxicants that mainly accumulate in the lungs. As a regulator of gene expression, microRNAs (miRNAs) were involved in some lung diseases. This study aimed to analyze the levels of some inflammatory cytokine and the differential expressions of miRNAs in human bronchial epithelial cells (16HBE) induced by beryllium sulfate (BeSO 4 ) and to further explore the biological functions of differentially expressed miRNAs. The profile of miRNAs in 16HBE cells was detected using the high-throughput sequencing between the control groups ( n = 3) and the 150 μmol/L of BeSO 4 -treated groups ( n = 3). Bioinformatics analysis of differentially expressed miRNAs was performed, including the prediction of target genes, Gene Ontology (GO) analysis, and the Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis. Quantitative real-time polymerase chain reaction (qRT-PCR) was applied to verify some damage-related miRNAs. We found that BeSO 4 can increase the levels of some inflammatory cytokine such as interleukin-10 (IL-10), tumor necrosis factor-alpha (TNF-α), interferon-γ (IFN-γ), inducible nitric oxide synthase (iNOS), and cyclooxygenase-2 (COX-2). And BeSO 4 altered miRNAs expression of 16HBE cells and a total of 179 differentially expressed miRNAs were identified, including 88 upregulated miRNAs and 91 downregulated miRNAs. The target genes predicted by 28 dysregulated miRNAs were mainly involved in the transcription regulation, signal transduction, MAPK, and VEGF signaling pathway. The qRT-PCR verification results were consistent with the sequencing results. miRNA expression profiling in 16HBE cells exposed to BeSO 4 provides new insights into the toxicity mechanism of beryllium exposure.
研究领域:
毒理学
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分子生物学
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生物信息学
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细胞生物学
✓ 已验证
DOI
PubMed
高影响因子
LIFE SCIENCES
·
2024
·
IF 5.2
Min Qiu,Liangyan Cheng,Jianbo Xu,Minwei Jin,Wenhua Yuan,Qinwen Ge,Kaiao Zou,Jiali Chen,Yuliang Huang,Ju Li,Liming Zhu,Bing Xu,Chunchun Zhang,Hongting Jin,Pinger Wang
Aims The main pathological features of osteoarthritis (OA) include the degeneration of articular cartilage and a decrease in matrix synthesis. Chondrocytes, which contribute to matrix synthesis, play a crucial role in the development of OA. Liquiritin, an effective ingredient extracted from Glycyrrhiza uralensis Fisch., has been used for over 1000 years to treat OA. This study aims to investigate the impact of liquiritin on OA and its underlying mechanism. Materials and methods Gait and hot plate tests assessed mouse behavior, while Micro-CT and ABH/OG staining observed joint morphological changes. The TUNEL kit detected chondrocyte apoptosis. Western blot and immunofluorescence techniques determined the expression levels of cartilage metabolism markers COL2 and MMP13, as well as apoptosis markers caspase3, bcl2, P53, and PUMA. KEGG analysis and molecular docking technology were used to verify the relationship between liquiritin and P53. Key findings Liquiritin alleviated pain sensitivity and improved gait impairment in OA mice. Additionally, we found that liquiritin could increase COL2 levels and decrease MMP13 levels both in vivo and in vitro. Importantly, liquiritin reduced chondrocyte apoptosis induced by OA, through decreased expression of caspase3 expression and increased expression of bcl2 expression. Molecular docking revealed a strong binding affinity between liquiritin and P53. Both in vivo and in vitro studies demonstrated that liquiritin suppressed the expression of P53 and PUMA in cartilage. Significance This indicated that liquiritin may alleviate OA progression by inhibiting the P53/PUMA signaling pathway, suggesting that liquiritin is a potential strategy for the treatment of OA.
研究领域:
药理学
·
骨科
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细胞生物学
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分子生物学
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生物医学工程
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DOI
PubMed
高影响因子
Antioxidants
·
2024
·Vol. 13
·期 9
·1026
·
IF 6
Dajin Pi,Zheng Liang,Jinyue Pan,Jianwei Zhen,Chuiyang Zheng,Wen Fan,Qingliang Song,Maoxing Pan,Qinhe Yang,Yupei Zhang
Nonalcoholic steatohepatitis (NASH) is a critical stage in the progression of nonalcoholic fatty liver disease (NAFLD). Tanshinone IIA (TIIA) is a tanshinone extracted from Salvia miltiorrhiza; due to its powerful anti-inflammatory and antioxidant biological activities, it is commonly used for treating cardiovascular and hepatic diseases. A NASH model was established by feeding mice a methionine and choline-deficient (MCD) diet. Liver surface microblood flow scanning, biochemical examination, histopathological examination, cytokine analysis through ELISA, lipidomic analysis, transcriptomic analysis, and Western blot analysis were used to evaluate the therapeutic effect and mechanism of TIIA on NASH. The results showed that TIIA effectively reduced lipid accumulation, fibrosis, and inflammation and alleviated endoplasmic reticulum (ER) stress. Lipidomic analysis revealed that TIIA normalized liver phospholipid metabolism in NASH mice. A KEGG analysis of the transcriptome revealed that TIIA exerted its effect by regulating the PPAR signalling pathway, protein processing in the ER, and the NOD-like receptor signalling pathway. These results suggest that TIIA alleviates NASH by activating the PPARα/FGF21 axis to negatively regulate the ER stress-induced unfolded protein response (UPR).
研究领域:
药理学
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肝病学
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分子生物学
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产品关联
DOI
PubMed
高影响因子
JOURNAL OF PHARMACEUTICAL AND BIOMEDICAL ANALYSIS
·
2024
·
IF 3.1
Jiayue Wang,Feixu Qin,Hongjin Wang,Lu Wang,Caihong Li,Lixin Sun
Senecio scandens Buch.-Ham., a traditional Chinese medicine commonly used clinically, exhibits various pharmacological properties, including anti-inflammatory, anti-tumor, antiviral, and antibacterial activities. However, its water extracts' chemical components and metabolites are inadequately understood, limiting further research. In this study, the chemical components and metabolism processes of Senecio scandens, both in vivo (plasma, feces, urine, and bile) and in vitro (gut microbiota and liver microsomes), were characterized based on ultra-high performance liquid chromatography coupled with hybrid quadrupole-orbitrap high-resolution mass spectrometry. Additionally, metabolites detectable in fecal samples and intestinal microbiota incubated but absent in liver microsomes were identified as characteristic metabolites of intestinal microbiota. The targets of the characteristic metabolites of intestinal microbiota were collected, followed by exploration of potential pathways through KEGG enrichment analysis. As a result, a total of 133 chemical components were preliminarily identified, including 35 organic acids, 21 alkaloids, 19 flavonoids and their glycosides, 17 phenylpropanoids, 10 jacaranda ketones, and 31 other compounds. Notably, 12 of these were potentially novel compounds. In addition, 39 prototype components in rats and 109 metabolites were identified and characterized, including 102 in vivo and 52 metabolites in vitro (51 in rat gut microbiota and 24 in rat liver microsomes). The main metabolic pathways include oxidation, reduction, hydrolysis, methylation, glucuronidation, sulfonation, and acetylation reactions. Furthermore, KEGG enrichment analysis revealed that the characteristic metabolites of intestinal microbiota may be related to the ErbB, FoxO, mTOR, and MAPK signaling pathways, exhibiting anti-inflammatory and anti-tumor effects. In summary, the chemical components and metabolites of Senecio scandens were comprehensively identified using a rapid and accurate method, providing a scientific basis for the in-depth study of the material basis and its clinical application of Senecio scandens .
研究领域:
药理学
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代谢组学
·
生物信息学
·
中药学
·
化学生物学
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微生物学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
BIOORGANIC CHEMISTRY
·
2020
·
IF 4.831
Zili Lei,Yanhong Yang,Shaomin Liu,Yuting Lei,Lanxiang Yang,Xueying Zhang,Wanwan Liu,Huijuan Wu,Changyuan Yang,Jiao Guo
In the present study, the effects of dihydroartemisinin (DHA) on inflammatory bowel diseases (IBD) mice model induced by dextran sulfate sodium (DSS) were determined. Hematoxylin and eosin staining was used to assess the intestines of mice treated with DSS and DHA. The expression of inflammatory factors and cell junction-associated genes was measured using reverse transcription-quantitative PCR (RT-qPCR) and Western blot. The effects of DSS and DHA on the gut microbiome were measured using 16S recombinant (r) DNA gene analysis. DHA could improve the diarrhea and bloody stool induced by DSS, and decrease the serum levels of TNF-α, IL-1β and IL-23 of the DSS group. DHA could notably reduce the infiltration of the inflammatory cells and significantly decrease the expression of TNF-α and IL-1β in the intestines of the DSS treated mice. The expression of cell junction-associated genes such as EpCAM and Claudins, were down-regulated in the DSS group, and DHA could recover the expression of these cell junction-associated genes. The 16S rDNA gene analysis demonstrated that Bacteroidetes and Verrucomicrobia decreased, while Firmicutes and Proteobacteria increased in the DSS group, and DHA could recover the abundance of these gut bacteria altered by DSS. The Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis revealed that DHA could partly recover the pathways altered by DSS. DHA could obviously ameliorate the symptoms of IBD induced by DSS by regulation of the expression of inflammation and cell junction-associated genes and gut microbiota, suggesting its potential for the treatment of IBD.
研究领域:
药理学
·
免疫学
·
胃肠病学
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微生物学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
危险品化学品经营许可证（带存储）