Annals of Translational Medicine
·
2022
·
IF 3.616
Lei Wang,Yanling Ding,Yanhui Bai,Jian Shi,Jia Li,Xiuli Wang
Background The lung is one of the most sensitive organs, and is vulnerable to injury caused by limb ischemia-reperfusion (LIR). Dexmedetomidine, an anesthetic adjunct, has been shown to have therapeutic effects on lung injury secondary to LIR. This study aimed to investigate the role of dexmedetomidine in ameliorating LIR-induced lung injury in a mouse model of bilateral hind LIR. Methods In this study, 75 mice were randomly divided into 5 groups to prepare the LIR model. After the model was established, arterial blood was extracted for blood gas analysis. The pathological changes of lung tissue, lung wet/dry weight ratio, arterial blood gas analysis, detection of myeloperoxidase (MPO) activity, the content of reactive oxygen species (ROS), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and malondialdehyde (MDA) in oxidative stress indexes, mitochondrial membrane potential (MMP), adenosine triphosphate (ATP) content and cytochrome c content were measured, and the relative protein expression levels of sirtuin-3 (SIRT3) and apoptosis factor Bcl-2 related X protein (Bax), B-cell Lymphoma 2 (Bcl-2), cleaved caspase 3, and nuclear factor erythroid 2-related factor 2 (Nrf2) and cytoplasmic heme oxygenase-1 (HO-1). Results Pretreatment with dexmedetomidine dramatically ameliorated LIR-induced lung injury, the wet/dry weight ratio, the arterial blood gas parameters, and enhanced SIRT3 expression. Moreover, dexmedetomidine significantly inhibits ROS and MDA level and restores antioxidant enzyme activities (SOD, GSH-Px). Of note, dexmedetomidine suppressed LIR-induced lung tissue apoptosis by modulating apoptosis-associated protein such as Bax, Bcl-2, and cleaved caspase 3. Moreover, dexmedetomidine inhibited the LIR-induced decreases in MMP, ATP levels, and the release of cytochrome c of LIR to maintain mitochondrial function. Latest study has shown that activating Nrf2 could promote SIRT3 expression to alleviate IR injury. Intriguingly, dexmedetomidine could facilitate nuclear Nrf2 and cytoplasmic HO-1 expression. Conclusions Our findings suggest that dexmedetomidine protects against LIR-induced lung injury by inhibiting the oxidative response, mitochondrial dysfunction and apoptosis. The mechanism appears to be at least partly mediated through the upregulation of SIRT3 expression.
研究领域:
药理学
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病理生理学
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呼吸医学
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分子生物学
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DOI
PubMed
高影响因子
Annals of Translational Medicine
·
2021
·
IF 3.932
Su-Su Tang,Shu-Yun Xing,Xue-Jiao Zhang,Xiao-Qian Ren,Hao Hong,Yan Long
Background Cognitive impairment is a serious complication of diabetes that manifests as an impairment of spatial memory and learning ability. Its pathogenesis is unclear, and effective therapeutic drugs are very limited. Our group designed and synthesized a novel compound named 3-p-tolyl-9H-xanthen-9-one (Tozan). In this study, we sought to investigate the effects and mechanism of Tozan on diabetic cognitive impairment. Methods Methylglyoxal (MG)-induced SH-SY5Y cells and streptozotocin (STZ)-induced type 1 diabetic mice were treated with Tozan. Methyl thiazolul tetrazolium (MTT) and lactate dehydrogenase (LDH) were used to test cytotoxicity. Morris water maze (MWM) and Y-maze tests were used to evaluate cognitive function. Immunofluorescence and western blot analyses were used to evaluate neurogenesis, apoptosis, and signal transduction pathway-related proteins. In addition, Lentivirus (LV)-estrogen receptor beta (ERβ)-ribonucleic acid interference (RNAi) was used to knockdown the ERβ gene in SH-SY5Y cells. Results We found that Tozan ameliorated MG-induced cytotoxicity in SH-SY5Y cells, improved cognitive dysfunction in STZ-induced type 1 diabetic mice, increased neurogenesis, and prevented apoptotic responses in vitro and in vivo . Importantly, Tozan (2, 4, and 8 mg/kg) mediated phosphatidylinositol-3-kinase and protein kinase B cAMP-response element binding protein (PI3K/Akt-CREB) signaling by activating membrane ERβ, and a high dose of Tozan (8 mg/kg) mediated CREB signaling by activating nuclear ERβ in the hippocampus. Notably, Tozan did not have an anti-apoptosis and regeneration protective role in ERβ gene knockdown cells. Conclusions Our study demonstrates Tozan’s contributions to and role in cognition, neurogenesis, and apoptosis in diabetes, and lays an experimental foundation for the development of new anti-diabetic cognitive impairment drugs.
研究领域:
药理学
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神经科学
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糖尿病研究
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细胞生物学
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DOI
PubMed
高影响因子
Annals of Translational Medicine
·
2020
·Vol. 8
·期 22
·1553
·
IF 3.297
Giacomo Savini,Leonardo Taroni,Kenneth J Hoffer
For many decades only a few formulas have been available to calculate the intraocular lens (IOL) power for patients undergoing cataract surgery: the Haigis, Hoffer Q, Holladay 1 and 2 and SRK/T. In recent years, several new formulas for IOL power calculation have been introduced with the aim of improving the accuracy of refraction prediction in eyes undergoing cataract surgery. These include the Barrett Universal II, the Emmetropia Verifying Optical (EVO), the Kane, the Næser 2, the Olsen, the Panacea, the Pearl DGS, the Radial Basis Function (RBF), the T2 and the VRF formulas. Although most of them are unpublished so that their structure is unknown, we give an overview of each formula and report the results of the studies that have compared them. Their performance in short and long eyes is provided and a special focus is given on the issue of segmented axial length, which is a promising method to obtain more accurate outcomes in short and long eyes. Here, the group refractive index originally developed for the IOLMaster may not represent the best method to convert the optical path length into a physical distance. The issue of posterior and total corneal astigmatism (TCA) is discussed in relation to toric IOLs; the latest formulas for toric IOLs and their results are also reported.
研究领域:
眼科学
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白内障手术
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屈光手术
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生物测量
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光学设计
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临床预测模型
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DOI
PubMed
高影响因子
Annals of Translational Medicine
·
2021
·
IF 3.932
Tingting Xu,Pei Wang,Xue Zheng,Zhanpeng Yan,Kun Li,Jindi Xu,Cuihua Jiang,Fangshi Zhu
Background Long Chai Fang (LCF) is a traditional Chinese medicine (TCM) formula for treating chronic hepatitis B (CHB) in clinical settings; however, its related mechanism remains unclear. Methods To address this issue, network pharmacology and an integrative method that combines dot-blot hybridization and metabolomics analysis were employed. Network pharmacology was performed to investigate the material basis and potential mechanisms of LCF against CHB. The effect of LCF on Duck hepatitis B virus (DHBV) replication was evaluated. The metabolomics analysis was conducted to identify potential biomarkers in duck serum. Results The network pharmacology approach revealed 133 potential active components, 897 drug targets, 979 disease targets, and 185 drug-disease targets, while the Kyoto Encyclopedia of Genes and Genomes enrichment analysis identified 165 pathways. LCF significantly inhibited DHBV-deoxyribonucleic acid replication on day 10 and day 3 after the cessation of treatment. Notably, the low-dose LCF group showed the best inhibitory effect. The obviously sustained anti-DHBV activity of LCF inhibited viral replication, and a rebound reaction was found. Phosphatidylcholine and phosphatidylethanolamine classes, which are mainly involved in liver cell repair and energy metabolism through phospholipid metabolic pathways, were identified by metabolomics analysis. Conclusions our results showed that the main active ingredients of LCF appear to be metacarpi, isorhamnetin, glypallichalcone, and phaseolinisoflavan. This study provides novel strategies for using a LCF formula against CHB in future research.
研究领域:
中药学
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病毒学
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药理学
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代谢组学
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产品关联
DOI
PubMed
高影响因子
Annals of Translational Medicine
·
2021
·
IF 3.932
Jing Lu,Wenjie Tian,Linxian Cui,Bing Cai,Tingting Zhang,Nan Huang,Lei Lu,Tao Zhu
Background Lidocaine (LDC) is a local anesthetic widely used to relieve intubation-related airway responses. However, low drug concentration and short effective duration of LDC is inadequate to provide a satisfactory anesthetic effect on the surface of the airway. The present study sought to develop a LDC-delivery endotracheal tube (ETT) to achieve high local drug concentration and sustained drug release with the aim of attenuating an intubation-related airway response. Methods ETTs and polyvinyl chloride (PVC) discs were coated with different molecular weight (MW) poly lactic-co-glycolic acid (PLGA: 50/50; MW: 3,000, 6,000, and 10,000) loaded with LDC by airbrush spray. The morphology of LDC-eluting coatings was analyzed using scanning electron microscopy. In vitro drug release was determined by ultraviolet spectrophotometer. An in vivo study was performed to investigate the differences in plasma LDC concentration, intubation tolerance, and tracheal tissue injury in rabbits undergoing intubation of blank, LDC-spray, or LDC-coated ETTs. Results Approximate 5 mg/cm 2 coatings (containing 2.5 mg/cm 2 LDC) were deposited onto the PVC discs and ETTs. While even distribution and smooth surfaces were generated in PLGA3000 + LDC and PLGA6000 + LDC coatings, PLGA10000 + LDC formed uneven and gullied coatings. Burst release within the first 4 h and sustained release for at least 5 days was achieved in vitro in PLGA + LDC coatings and the in vivo study demonstrated higher plasma LDC concentration and longer drug release duration in LDC-coated ETTs compared with LDC-spray. LDC-coated ETTs significantly improved intubation tolerance in rabbits, as measured by less general anesthetic consumption and longer tube tolerance duration in contrast to blank ETTs with or without LDC spray. Histology assessment showed less mucosal edema area in the PLGA3000 + LDC and PLGA6000 + LDC groups compared to the control, LDC-spray, and PLGA10000 + LDC groups. Among the different MW PLGAs, PLGA6000 presented optimal morphological characteristics, drug release, and anesthetic effect. Conclusions ETTs coated with PLGA + LDC effectively attenuate an intubation-related airway response via increasing local drug concentration and extending drug action duration, which demonstrates a potential therapeutic benefit for patients undergoing intubation.
研究领域:
麻醉学
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药剂学
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生物医学工程
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产品关联
DOI
PubMed
高影响因子
Annals of Translational Medicine
·
2020
·
IF 3.297
Li-Xuan Yang,Fang-Yu Chen,Hai-Long Yu,Pin-Yi Liu,Xin-Yu Bao,Sheng-Nan Xia,Yue Gu,Yun Xu,Xiang Cao
Background Based on accumulating evidence, excessive activation of microglia-mediated inflammatory responses plays an essential role in ischemic stroke. Poncirin (Pon) exerts anti-hyperalgesic, anti-osteoporotic and anti-tumor effects on various diseases. However, the roles of Pon in microglial activation and the underlying mechanism have not been elucidated. This study aimed to explore whether Pon inhibits lipopolysaccharide (LPS)-induced microglial neuroinflammation and protects against brain ischemic injury in experimental stroke in mice. Methods Primary microglia cells were prepared from the cerebral cortices of 1- to 2-day-old C57BL/6J mice. Murine BV2 cells and primary microglia were stimulated with LPS and the effects of a non-cytotoxic concentration of Pon on LPS-stimulated pro-inflammatory factors were measured using real-time PCR and enzyme-linked immunosorbent assays (ELISAs). Western blot analyses were used for mechanistic studies. In an in vivo study, 8-week-old male C57BL/6J mice were subjected to focal cerebral ischemia through middle cerebral artery occlusion (MCAO). Pon (30 mg/kg, i.p.) or the same volume of saline was administered after the MCAO model was established, and the infarct volume was evaluated using 2,3,5-triphenyltetrazolium chloride (TTC) staining. We also evaluated animal behaviours, the expression of pro-inflammatory cytokines and microglial activation in the ischemic hemisphere. Results Pon prevented the release of nitric oxide (NO), prostaglandin E2 (PGE2), interleukin (IL)-1β, IL-6 and tumor necrosis factor-alpha (TNF-α) in both BV2 cells and primary microglia stimulated with LPS. The inhibitory effects of Pon were associated with the regulation of the ERK1/2, JNK and nuclear factor kappa B (NF-κB) signaling pathways. In mice that underwent MCAO, Pon administration decreased the lesion size and improved neurological deficits. Furthermore, Pon attenuated the production of inflammatory cytokines mainly by restraining microglial activation after ischemic stroke. Conclusions Based on the findings from the present study, Pon provides neuroprotection through its anti-inflammatory effects on microglia and it may be a useful treatment for ischemic stroke.
研究领域:
神经科学
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药理学
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免疫学
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神经病学
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产品关联
DOI
PubMed
高影响因子
Annals of Translational Medicine
·
2021
·
IF 3.932
Xiangrui Meng,Yuanyuan Sun,Lan Wang,Yuhao Li,Ruizhuo Ouyang,Ping Yuan,Yuqing Miao
Background Under hypoxic conditions, the brain can undergo irreversible damage. The present study aimed to explore new higher-oxygen-content carbamide peroxide (CP) compounds and the effect of their oxygen-releasing property on human brain microvascular endothelial cell (EC) proliferation under in vitro hypoxic conditions. Methods Two different additives including alpha-terpineol and sorbic acid were added to the reaction system to obtain the carbamide peroxide of CP-I and CP-II. Results We evaluated the oxygen generation capabilities of CP samples by using a portable dissolved oxygen meter. Consequently, alpha-terpineol as a stabilizer exhibited a unique effect on the oxygen generation of CP. CP-I was uniquely able to promote cell proliferation ability at 10 µg·L −1 for hypoxic conditions, with the proliferation rates being 36.2% compared with the control group. The safety of CP to cells was further verified by calcein-AM/PI staining. Under hypoxic conditions, CP-I at 10 µg·L −1 promoted the migration rate, and the migration rate being 32.37%. Conclusions These compounds have the advantages of simple synthesis, long storage time, low cost, and rich oxygen content. Used spectrophotometry, oxygen electrode test, and indicator titration for testing the oxygen production rate and oxygen production. The results indicate that alpha-terpineol is the best additive. CP-I exhibited the highest oxygen content and a superior effect on the cell phenotype than CP-II, especially under hypoxia. This study is the first to report the effects of CP on cells, and provides new therapeutic insights into cerebrovascular injury repair.
研究领域:
神经生物学
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细胞生物学
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药理学
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产品关联
DOI
PubMed
高影响因子
Annals of Translational Medicine
·
2020
·
IF 3.297
Li Li,Xingfeng He,Xingtong Wang,Yu Sun,Guosheng Wu,He Fang,Chen Wang,Pengfei Luo,Zhaofan Xia
Background Ruxolitinib is an inhibitor of Janus kinases (JAK) 1/2. It was authorised recently by the U.S. Food and Drug Administration (FDA) as a new Myelofibrosis treatment. In this study, we identified ruxolitinib as a new inhibitor of nitric oxide (NO) production in response to lipopolysaccharide (LPS)stimulation of RAW 264.7 cells. Methods In vitro direct effects of ruxolitinib were determined through NO production on RAW 264.7 cells. Also the expression level of iNOS, TNF-α and IL-6 were detected by Western Blotting and qRT-PCR. In vivo therapeutic effects of ruxolitinib on sepsis were evaluated by an endotoxemia model with C57 mice. The survival was calculated and histopathological damage of organs was observed by HE. Cytokines in serum were detected by Mouse Cytokine Array Panel. Results Ruxolitinib was found to significantly reduce NO production, inducible nitric oxide synthase (iNOS), TNF-α, and IL-6 expression, suggesting that ruxolitinib blocks LPS signaling that leads to pro-inflammatory factor expression. Furthermore, the inhibitory effects of ruxolitinib contributed to the survival of septic mice by 70% and pro-inflammatory cytokines in serum declined apparently. The results taken together indicate that ruxolitinib can significantly suppress LPS-stimulated NO production and improve the survival of septic mice, perhaps by interfering with the NF-κB pathway. Conclusions These findings suggest ruxolitinib might be a possible therapeutic candidate for sepsis therapy.
研究领域:
药理学
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免疫学
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传染病学
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产品关联
DOI
PubMed
高影响因子
Annals of Translational Medicine
·
2022
·
IF 3.616
Huili Huang,Ying Tong,Tong Fu,Danmei Lin,Hansheng Li,Li Xu,Senyue Zhang,Yanzhe Yin,Yiran Gao
Background To use network pharmacology and gut microbiota sequencing to investigate the probable mechanism of Bining decoction (BN) in the treatment of gouty nephropathy (GN). Methods Firstly, the mechanism of therapeutic effects of BN on GN were collected by integrating network pharmacology. Secondly, the treatment effects of BN against GN in 30 Institute of Cancer Research (ICR) mice were evaluated by performing biochemical tests [uric acid, blood urea nitrogen, and creatinine (UA, BUN, and Cr)] and evaluating the renal weight index. Finally, 16S rRNA sequencing was utilized for elucidating the therapeutical effect of BN in GN. Results The results of gut microbiota sequencing analysis showed the abundance of Faecalibaculum , Romboutsia , Bifidobacterium , Bacteroides , Odoribacter , Lachnospiraceae NK4A136 group, unclassified_f__ Lachnospiraceae , Roseburia , norank_f__ Lachnospiraceae , Lactobacillus , Dubosiella , norank_f__ Muribaculaceae , and Turicibacter in the BN group had a significant changed between-group comparisons. Using a network pharmacology-related database, 413 active components of BN were identified, as well as 1,085 GN-associated targets. The 118 targets of disease targets and component targets were mapped, of which the top 10 genes were selected. The Kyoto Encyclopedia of Genes and Genomes (KEGG) results showed that 157 pathways were enriched, which was partially consistent with the metabolic pathways of gut microbiota sequencing analysis. Conclusions Combining 16S rRNA gene sequencing and network pharmacology analysis, similar signaling pathways were followed: “Pathways in cancer” and “Adipocytokine signaling pathway”. The results reveal that BN increases the abundance of Turicibacter , regulates the expression of JAK2 in the JAK/STAT pathway, increases the beneficial bacteria Turicibacter associated with intestinal butyric acid, which could enhance the intestinal barrier, and exert anti-inflammatory effects.
研究领域:
药理学
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微生物学
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分子生物学
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肾病学
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产品关联
DOI
PubMed
高影响因子
Annals of Translational Medicine
·
2022
·
IF 3.616
Weidong Li,Lisha Li,Fujie Yang,Qiongying Hu,Daqian Xiong
Background The relationship between gut microbiota and metabolites play an important role in the occurrence and development of type 2 diabetes mellitus (T2DM). However, the interaction between intestinal flora abundance and metabolites is still unclear. The purpose of this study was to investigate the correlation of the interaction network between intestinal flora and fecal metabolites in regulating the occurrence of T2DM. Methods This a case-control study. T2DM patients with different glucose levels and healthy people were divided into case group and normal controls (NC) group. Fasting plasma and fecal samples were collected from the subjects. Ultra-performance liquid chromatography-tandem mass spectrometry (LC-MS) untargeted fecal metabolomics was used to detect small molecular metabolites within 1,500 Da in two groups. The diversity and richness of intestinal flora were analyzed by the 16SrRNA third-generation full-length sequencing technique and the correlation between intestinal microflora and different metabolites was evaluated. Results A total of 30 patients with T2DM and 21 NC were included for analysis, glycated hemoglobin (HbAlc) (P<0.001), fasting blood glucose (FBG) (P<0.001), total triglycerides (TG) (P=0.002), and fasting serum insulin (FINS) (P=0.026) were significantly higher in the T2DM group compared with the NC group. The fecal metabolomics profiles of the T2DM group and NC group were significantly different, and 355 different metabolites were identified among the two. Compared with the NC group, the levels of ornithine (P=0.04), L-lysine (P=0.03), glutamate (P=0.01), alpha-linolenic acid (P=0.004), traumatin (P=0.05), and erucic acid (P=0.004) in the T2DM group decreased significantly, while PC[18:3(6Z,9Z,12Z)/24:1(15Z)] (P<0.001) levels increased. Compared with the NC group, the richness of Megamonas and Escherichia increased in T2DM patients, while that of Bacteroidota and Phascolarctobacterium were lower. Pearson correlation analysis revealed associations between gut microbiota and faecal metabolites, and Phascolarctobacterium was positively correlated with alpha-linolenic acid (r=0.72, P<0.001). Conclusions There may be a mutual regulatory network between intestinal bacteria and fecal metabolites in T2DM. The increased abundance of Phascolarctobacterium may increase alpha-linolenic acid uptake, and alpha-linolenic acid may also increase the abundance of intestinal Phascolarctobacterium in vivo after metabolic transformation. The combination of the two may play an important role in the treatment of diabetes.
研究领域:
医学
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微生物学
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代谢组学
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DOI
PubMed
高影响因子
NEUROENDOCRINOLOGY
·
2023
·Vol. 113
·期 6
·641-656
·
IF 4.1
Zheng Biaolin,Chen Xiubing,Chen Fengping,Liao Xiaomin,Wang Feng,Yang Zhe,Yi Nan,Shi Xiaoyan,Qin Shanyu,Jiang Haixing
Introduction: 5-Iodotubercidin, a type of purine derivative, has attracted increasing attention in tumor chemotherapy because of its potential as an antitumor agent in recent years. In this study, we confirmed the effects on apoptosis in insulinoma cell lines induced by 5-iodotubercidin and tried to illuminate the underlying mechanisms. Methods: We used 5-iodotubercidin in the treatment of insulinoma cells and the cell proliferation was examined using CCK-8 assay, colony-forming assays, and insulinoma animal models. Cell apoptosis was examined using TUNEL assays and Western blotting. Cellular DNA damage was shown by comet assay and immunofluorescence. The expression of apoptosis-regulating proteins and DNA damage biomarker was investigated by Western blotting. Subcutaneous inoculation of the insulinoma cells into nude mice was to measure blood glucose, insulin levels, and tumor growth. ATM siRNA and p53 siRNA were used as loss-of-function targets to evaluate 5-iodotubercidin treatment. Results: 5-Iodotubercidin inhibited the proliferation of insulinoma cells and induced DNA damage and cell apoptosis. Moreover, 5-iodotubercidin induced ATM and p53 activated. In vivo, 5-iodotubercidin inhibited the growth of Ins-1 and Min-6 cells xenografts in nude mice. Conclusion: 5-Iodotubercidin induces DNA damage leading to insulinoma cells apoptosis by activating ATM/p53 pathway. Therefore, this is a potential strategy for treating insulinoma
研究领域:
肿瘤学
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分子生物学
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细胞生物学
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药理学
✓ 已验证
DOI
PubMed
高影响因子
Italian Journal of Animal Science
·
2021
·
IF 2.217
Yi Ma,Mawda Elmhadi,Chao Wang,Hao Zhang,Hongrong Wang
Several studies have demonstrated that high-concentrate (HC) diet with thiamine supplementation can alleviate rumen epithelium inflammation and protecting the barrier function in goats. This study aimed to investigate the effects of dietary supply of thiamine on mitophagy and endoplasmic reticulum stress (ERS) during high-concentrate diet feeding. Twenty-four Boer goats (35.62 ± 2.4 kg) were used in this study, goats were subsequently assigned to 3 treatment groups (8 goats in each group) as follows: a low-concentrate diet (CON; concentrate: forage 30:70), a high-concentrate diet (HC; concentrate: forage 70:30) and high-concentrate diet with 200 mg thiamine/kg DMI (HCT; concentrate: forage 70:30) for 12 weeks. Compared with the HC group, the goats of HCT group had a markedly higher final weight, net weight gain, and average daily gain (ADG). The blood physiological and biochemical results showed that the HCT group expressed a lower the content of lymphocytes and leukocytes but a higher total protein and monocytes compared with that of HC group. The rumen epithelial mitochondrial membrane potential change (ΔΨm), relative mitochondrial DNA (mtDNA) content, adenosine triphosphate (ATP) level, together with the activities of the respiratory complexes I, III, and IV were markedly higher in the HCT group relative to HC ones. Relative to the HC group, the unc-51 like autophagy activating kinase 1 (ULK1), microtubule-associated protein 1 light chain 3 (LC3), autophagy-related 5 (ATG5), autophagy related 7 (ATG7), Beclin1, PTEN induced putative kinase 1 (PINK1), PERK (PKR-Endoplasmic Reticulum Kinase), activating transcription factor 4 (ATF4), activating transcription factor 6 (ATF6), X-box binding protein 1 (XBP1), heat shock 70 kDa protein 5 (HSPA5), DNA damage-inducible transcript 3 (DDIT3) and DNA damage-inducible transcript 4 (DDIT4) mRNA levels were decreased, but the breast cancer 1 (BRCA1), ataxia telangiectasia mutated (ATM), heat shock factor binding protein 1 (HSBP1) were increased in rumen epithelium of the HCT group. The results of transmission electron micrographs showed that the cell structure of the HCT group was higher integrity than that in the HC group, and the damage degree of mitochondria as well as endoplasmic reticulum being lower than the HC group. These results demonstrated that dietary thiamine could enhance rumen epithelial integrity by suppressing the responses of ERS and mitophagy during long-term HC diet feeding.HIGHLIGHTSThis study is the first to demonstrate that the reduction of inflammatory response is related to the down-regulation of autophagy and endoplasmic reticulum stress in goats.Thiamine has good anti-inflammatory and anti-oxidation properties, which can be applied in intensive industry to reduce the negative effects caused by long-term high-concentrate diet.
研究领域:
动物营养
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分子生物学
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兽医学
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营养基因组学
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产品关联
DOI
高影响因子
危险品化学品经营许可证（带存储）