Revealing improvement mechanism of yak meat quality by dietary with Codonopsis pilosula stems and leaves based on transcriptomics and metabolomics.

The present study was performed to investigate the effects of dietary supplementation with herbal additives on meat quality, slaughter performance and the cecal microbial community in Hungarian white geese. A total of 60 newborn geese were assigned equally into the control group (CON) and the herbal complex supplemented group (HS). The dietary supplementations consisted of Compound Herbal Additive A (CHAA) including Pulsatilla, Gentian and Rhizoma coptidis, and Compound Herbal Additive B (CHAB) containing Codonopsis pilosula, Atractylodes, Poria cocos and Licorice. The geese in the HS group received a basal diet supplemented with 0.2% CHAA from day 0 to day 42 at the postnatal stage. Then from day 43 to day 70, the geese in HS group were provide a basal diet with 0.15% CHAB. The geese in the CON group were only provided with the basal diet. The results showed that the slaughter rate (SR), half chamber rates (HCR), eviscerated rate (ER) and breast muscle rate (BMR) in the HS group tended to increase slightly compared with the CON group (ns). In addition, the shear force, filtration rate and pH value of breast muscle and thigh muscle in the HS group were slightly enhanced compared to the CON group (ns). Significant increased levels in carbohydrate content, fat content and energy (P<0.01) and significant decreased levels in cholesterol content (P<0.01) were observed in the muscle of the HS group. The total amino acid (Glu, Lys, Thr and Asp) content in the muscle increased in HS group than in the CON group (P<0.01). Dietary herb supplementations significantly increased the levels of IgG in serum (P<0.05) on day 43 and higher levels of IgM, IgA and IgG (P<0.01) were also observed in the HS group on day 70. Furthermore, 16S rRNA sequencing results indicated that herbal additives increased the growth of beneficial bacteria and inhibited the proliferation of harmful bacteria in the geese caecum. Altogether, these results offer crucial insights into the potential benefits of incorporating CHAA and CHAB into the diets of Hungarian white goose. The findings indicate that such supplementations could significantly improve meat quality, regulate the immune system and shape the intestinal microbiota composition.

Rapid profiling of fish cell nitrogen metabolism with single-cell Raman spectroscopy: Unveiling enzyme's role in ammonia detoxification

BackgroundTrimethylamine N-oxide (TMAO) is a metabolite produced by gut microbiota, and its potential impact on lipid metabolism in mammals has garnered widespread attention in the scientific community. Bovine fatty liver disease, a metabolic disorder that severely affects the health and productivity of dairy cows, poses a significant economic burden on the global dairy industry. However, the specific role and pathogenesis of TMAO in bovine fatty liver disease remain unclear, limiting our understanding and treatment of the condition. This study aims to construct a bovine fatty liver cell model using an integrated approach that combines transcriptomic, proteomic, and metabolomic data. The objective is to investigate the impact of TMAO on lipid metabolism at the molecular level and explore its potential regulatory mechanisms.ResultsWe established an in vitro bovine fatty liver cell model and conducted a comprehensive analysis of cells treated with TMAO using high-throughput omics sequencing technologies. Bioinformatics methods were employed to delve into the regulatory effects on lipid metabolism, and several key genes were validated through RT-qPCR. Treatment with TMAO significantly affected 4790 genes, 397 proteins, and 137 metabolites. KEGG enrichment analysis revealed that the significantly altered molecules were primarily involved in pathways related to the pathology of fatty liver disease, such as metabolic pathways, insulin resistance, hepatitis B, and the AMPK signaling pathway. Moreover, through joint analysis, we further uncovered that the interaction between TMAO-mediated AMPK signaling and oxidative phosphorylation pathways might be a key mechanism promoting lipid accumulation in the liver.ConclusionsOur study provides new insights into the role of TMAO in the pathogenesis of bovine fatty liver disease and offers a scientific basis for developing more effective treatment strategies.

Objective To explore the effect and mechanism of a new processing method of Codonopsis pilosula (CP) on the endocrine physique index in rats. Methods The rats were randomly assigned into the control group, model group, CP group (3.75 g/kg crude drug), rice-fried CP group (3.75 g/kg crude drug), and honey-roasted CP group (3.75 g/kg), with 10 rats in each group. All rats were gavaged according to the body weight of 1 mL/100 g every morning for 3 weeks. The water extracts of different processed products of CP were given to the drug group, the blank group, and the model group which were given the same volume of normal saline during the experiment. The model group and each administration group were fed every other day and drank freely for 21 days, during which the weight was weighed every 2 days. The changes of the organ index; the contents of cyclic adenosine monophosphate (cAMP), cyclic guanosine monophosphate (cGMP), adrenocorticotropic hormone (ACTH), and cortisol (Cor); and the activity of sodium and potassium adenosine triphosphate (Na+K+-ATP) were measured by enzyme-linked immunosorbent assay (ELISA). The expression of aquaporin-1 (AQP1) and aquaporin-2 (AQP2) mRNA was detected by RT-PCR. Results Effect on the organ index: the organ index of the control group, CP group, rice-fried group, and honey moxibustion group was higher compared to that of the model group, and the organ index of the honey moxibustion group was the highest (P < 0.05). The level of cAMP and the ratio of cAMP/cGMP in the model group were significantly higher compared to those of the control group (P < 0.05); CGMP in the model group decreased significantly (P < 0.05). Compared with the model group, the level of cAMP in the CP group, rice-fried group, and honey moxibustion group decreased significantly, while the ratio of cGMP and cAMP/cGMP increased significantly (P < 0.05). Compared with the CP group, rice-fried group, and honey moxibustion group, the level of cAMP and the ratio of cAMP/cGMP in the honey moxibustion group were lower compared to those in the other two groups, and the ratio of cGMP in the honey moxibustion group was higher compared to that in the other two groups (P < 0.05). The contents of ACTH and Cor in the model group were significantly higher compared to those in the control group (P < 0.05). Compared with the model group, the contents of ACTH and Cor in the CP group, rice-fried group, and honey moxibustion group were significantly lower compared to those in the model group (P < 0.05). Compared with the CP group, rice-fried group, and honey moxibustion group, the contents of ACTH and Cor in the honey moxibustion group were higher compared to those in the other two groups (P < 0.05). The content of the Na+K+-ATP enzyme in the model group was significantly higher compared to that in the control group (P < 0.05). Compared with the model group, the content of the Na+K+-ATP enzyme in the CP group, rice-fried group, and honey moxibustion group decreased significantly (P < 0.05). Compared with the CP group, rice-fried group, and honey moxibustion group, the content of the Na+K+-ATP enzyme in the honey moxibustion group was higher compared to that in the other two groups (P < 0.05). The expression of AQP1 and AQP2 mRNA in the kidney tissue of the kidney yin deficiency model group was significantly higher compared to that of the control group (P < 0 05). Compared with the model group, the expression levels of AQP1 and AQP2 mRNA in the renal tissue of rats in the CP group, rice-fried group, and honey moxibustion group decreased in different degrees (P < 0.05). There was no statistical difference between the CP group, rice stir-frying group, and honey moxibustion group. Conclusion This study proves that the new processing method of CP can improve the endocrine physique index of rats, enhance their organ quality, and regulate the disorder of water metabolism in kidney yin deficiency syndrome and has a certain therapeutic effect on kidney yin deficiency syndrome. Different new processing methods of CP have different effects on promoting endocrine physique indexes of rats. It is concluded that honey-roasted CP has the best effect on promoting spleen deficiency, which may be through glucose metabolism, amino acid metabolism, and nucleotide metabolism, increasing ATP energy metabolism, so as to strengthen the symptoms of spleen deficiency in rats. The experimental data of this study indicate that the effect of honey-roasted CP is better compared to that of other processed products, which provides an experimental basis for the rational clinical application of the new processed products.

Exposure to hypoxia disrupts energy metabolism and induces inflammation. However, the pathways and mechanisms underlying energy metabolism disorders caused by hypoxic conditions remain unclear. In the present study, a hypoxic animal model was created and transcriptomic and non-targeted metabolomics techniques were applied to further investigate the pathways and mechanisms of hypoxia exposure that disrupt energy metabolism. Transcriptome results showed that 3,007 genes were significantly differentially expressed under hypoxic exposure, and Gene Ontology annotation analysis and Kyoto Encyclopaedia of Genes and Genomes (KEGG) enrichment analysis showed that the differentially expressed genes (DEGs) were mainly involved in energy metabolism and were significantly enriched in the tricarboxylic acid (TCA) cycle and oxidative phosphorylation (OXPHOS) pathway. The DEGs IDH3A, SUCLA2, and MDH2 in the TCA cycle and the DEGs NDUFA3, NDUFS7, UQCRC1, CYC1 and UQCRFS1 in the OXPHOS pathway were validated using mRNA and protein expression, and the results showed downregulation. The results of non-targeted metabolomics showed that 365 significant differential metabolites were identified under plateau hypoxia stress. KEGG enrichment analysis showed that the differential metabolites were mainly enriched in metabolic processes, such as energy, nucleotide and amino acid metabolism. Hypoxia exposure disrupted the TCA cycle and reduced the synthesis of amino acids and nucleotides by decreasing the concentration of cis-aconitate, α-ketoglutarate, NADH, NADPH and that of most amino acids, purines, and pyrimidines. Bioinformatics analysis was used to identify inflammatory genes related to hypoxia exposure and some of them were selected for verification. It was shown that the mRNA and protein expression levels of IL1B, IL12B, S100A8 and S100A9 in kidney tissues were upregulated under hypoxic exposure. The results suggest that hypoxia exposure inhibits the TCA cycle and the OXPHOS signalling pathway by inhibiting IDH3A, SUCLA2, MDH2, NDUFFA3, NDUFS7, UQCRC1, CYC1 and UQCRFS1, thereby suppressing energy metabolism, inducing amino acid and nucleotide deficiency and promoting inflammation, ultimately leading to kidney damage.

The profiles of miRNAs and lncRNAs in peripheral blood neutrophils exosomes of diffuse cutaneous systemic sclerosis

The gut microbiota composition of sea cucumber ( Apostichopus japonicas ) was investigated using high-throughput sequencing techniques. The mRNA expression of complement component 3 and lysozyme genes was evaluated using quantitative fluorescence PCR. Sea cucumbers were fed with a basal diet (control group) and an experimental diet supplemented with Codonopsis pilosula (experimental group) for 30 days. The results showed that the alpha diversity of the gut microbiota was changed in different indices, including Chao1, the abundance-based coverage estimator, the Shannon index, and Good’s coverage. Dietary C. pilosula promoted the proliferation of the Flavobacteriaceae family of the Proteobacteria phylum and reduced the relative abundance of the Verrucomicrobiaceae family of the Verrucomicrobia phylum. We concluded that dietary C. pilosula supplementation could alter the network interactions among different microbial functional groups by changing the ecological network’s microbial community composition and biological evolution. A positive effect on A. japonicus immune responses in the gut was seen via increasing the mRNA expression of the complement component 3 and lysozyme genes. It seems to happen via modulating the balance in gut microbiota.

Examination of role of the AMP-activated protein kinase (Ampk) signaling pathway during low salinity adaptation in the mud crab, Scylla paramamosain, with reference to glucolipid metabolism

BackgroundAlzheimer's disease (AD) is the most common type of dementia and has a complex pathogenesis with no effective treatment. Energy metabolism disorders, as an early pathological event of AD,have attracted attention as a promising area of AD research. Codonopsis pilosula Polysaccharides are the main effective components of Codonopsis pilosula, which have been demonstrated to regulate energy metabolism.MethodsIn order to further study the roles and mechanisms of Codonopsis pilosula polysaccharides in AD, this study used an Aβ1-40-induced PC12 cells model to study the protective effects of Codonopsis pilosula polysaccharides and their potential mechanisms in improving energy metabolism dysfunction.ResultsThe results showed that Aβ1-40 induced a decrease in PC12 cells viability, energy metabolism molecules (ATP, NAD+, and NAD+/NADH) and Mitochondrial Membrane Potential (MMP) and an increase in ROS. Additionally, it was found that Aβ1-40 increased CD38 expression related to NAD+ homeostasis, whereas Silent Information Regulation 2 homolog1 (SIRT1, SIRT3), Peroxisome proliferator-activated receptor γ coactivator 1-α (PGC-1α) and SIRT3 activity were decreased. Codonopsis pilosula polysaccharides increased NAD+, NAD+/NADH, SIRT3, SIRT1, and PGC-1α related to NAD+, thus partially recovering ATP.ConclusionOur findings reveal that Codonopsis pilosula polysaccharides protected PC12 cells from Aβ1-40-induced damage, suggesting that these components of the Codonopsis pilosula herb may represent an early treatment option for AD patients.

Investigation of the effects of dichlorvos poisoning on AMPK signaling pathway in chicken brain tissues

Separation and identification of differential protein in rat's bone with fluorosis and calcium supplementation intervention

BackgroundNeuroinflammation and abnormal energy metabolism have been shown to significantly contribute to the progression of Alzheimer’s disease (AD). Adenylate kinase 5 (AK5), an enzyme predominantly expressed in the brain regulates ATP metabolism, has an unclear role in energy metabolism and neuroinflammation in AD.MethodsThe AD datasets were derived from the GEO public database to analyze the expression levels of AK5 in AD and normal samples and to assess the relationship between AK5 expression and the clinical characteristics of AD patients. Functional enrichment analysis was employed to investigate the effects of changes in AK5 expression on energy metabolism and immunoinflammation in AD, as well as the underlying mechanisms. Moreover, the influence of AK5 expression variations on oligodendrocyte development was assessed, and the predicted outcomes were validated through cellular experiments.ResultsBioinformatic analysis revealed that AK5 was lowly expressed in AD olfactory lobe tissues, accompanied by increased immunoinflammation and apoptosis. Increased expression of AK5 was associated with the activation of AMPK signaling, enhanced oxidative phosphorylation, and overall stimulation of energy metabolism. In oligodendrocytes treated with Aβ1-42, overexpression of AK5 resulted in elevated levels of P-AMPK, SIRT1, and BCL-2 proteins, while reducing the levels of BAX, CASPASE-3, and NF-κB proteins. This modulation activated AMPK signaling, thereby inhibiting neuroinflammation and apoptosis. In contrast, low levels of AK5 expression during early differentiation triggered inflammatory responses and increased apoptosis in oligodendrocytes.ConclusionAK5 inhibits AD oligodendrocyte apoptosis by activating the AMPK signaling pathway.

&lt;div&gt;Abstract&lt;p&gt;Metabolic reprogramming constitutes a key mechanism driving immunotherapy resistance in colorectal cancer although the immunomodulatory role of L-arginine metabolism remains poorly defined. Through metabolomic profiling, we identified aldehyde dehydrogenase 2 (ALDH2) as a critical regulator depleting intracellular L-arginine pools in colorectal cancer cells. High-performance liquid chromatography analysis of cell supernatants further demonstrated that ALDH2 overexpression significantly diminishes extracellular L-arginine availability. Functionally, this arginine deficiency suppressed CD8&lt;sup&gt;+&lt;/sup&gt; T-cell proliferation while inducing the attenuation of antitumor efficacy. Mechanistic studies revealed that ALDH2 upregulates pre–B-cell leukemia homeobox 3 (PBX3), which enhances arginase 2 (ARG2) transcription to promote L-arginine catabolism. This process suppresses glycolysis in CD8&lt;sup&gt;+&lt;/sup&gt; T cells, ultimately compromising their effector functions. Notably, ALDH2-high tumors exhibited resistance to immune checkpoint blockade (ICB), whereas combinatorial ARG2 inhibition and ICB therapy synergistically restored antitumor immunity. These findings nominate ARG2 as a novel therapeutic target and propose dual metabolic–immunologic intervention as a promising strategy for ICB-resistant colorectal cancer.&lt;/p&gt;&lt;/div&gt;

Metabolic reprogramming constitutes a key mechanism driving immunotherapy resistance in colorectal cancer although the immunomodulatory role of L-arginine metabolism remains poorly defined. Through metabolomic profiling, we identified aldehyde dehydrogenase 2 (ALDH2) as a critical regulator depleting intracellular L-arginine pools in colorectal cancer cells. High-performance liquid chromatography analysis of cell supernatants further demonstrated that ALDH2 overexpression significantly diminishes extracellular L-arginine availability. Functionally, this arginine deficiency suppressed CD8+ T-cell proliferation while inducing the attenuation of antitumor efficacy. Mechanistic studies revealed that ALDH2 upregulates pre-B-cell leukemia homeobox 3 (PBX3), which enhances arginase 2 (ARG2) transcription to promote L-arginine catabolism. This process suppresses glycolysis in CD8+ T cells, ultimately compromising their effector functions. Notably, ALDH2-high tumors exhibited resistance to immune checkpoint blockade (ICB), whereas combinatorial ARG2 inhibition and ICB therapy synergistically restored antitumor immunity. These findings nominate ARG2 as a novel therapeutic target and propose dual metabolic-immunologic intervention as a promising strategy for ICB-resistant colorectal cancer.

Effects of baicalin and chlorogenic acid on growth performance, slaughter performance, antioxidant capacity, immune function and intestinal health of broilers