Leptin pathway is a crucial target for anthocyanins to protect against metabolic syndrome.

The high prevalence of metabolic syndrome is threatening the health of populations all over the world. Contemporary work demonstrates that high leptin concentration is directly related to the development of metabolic syndrome such as obesity, fatty liver diseases, type 2 diabetes mellitus and cardiovascular diseases. Anthocyanins are a widespread group of dietary polyphenols, which can ameliorate chronic diseases related to metabolic syndrome. In addition, anthocyanins can regulate the leptin pathway in chronic metabolic diseases, however the potential mechanism between anthocyanin and leptin is complex and elusive. In this review paper, we have evaluated the bioactivity of anthocyanins on the mediation of leptin level and the upstream and downstream pathways in chronic metabolic diseases. Anthocyanins could regulate the hypertrophy of adipose tissue, and the expression of leptin level via mediating TNF-α, C/EBP, PPAR, CREB and SREBP-1. Anthocyanins promoted the leptin sensitivity by increasing the level of leptin receptor, phosphorylation of JAK2/STAT3, PI3K/AKT, and additionally ameliorated metabolic disorder related outcome, including oxidative stress, inflammation, lipid accumulation, insulin resistance and the balance of gut microbiota. However, direct evidence of anthocyanins treatment on leptin signal transduction is still limited which calls for future molecular binding and gene regulation test.

Natural antioxidants mitigate heavy metal induced reproductive toxicity: prospective mechanisms and biomarkers.

Heavy metals are harmful environmental pollutants that have attracted widespread attention, attributed to their health hazards to humans and animals. Due to the non-degradable property of heavy metals, organisms are inevitably exposed to heavy metals such as arsenic (As), cadmium (Cd), lead (Pb), and mercury (Hg). Several studies revealed that heavy metals can cause reproductive damage by the excessive production of reactive oxygen species (ROS), which exacerbates oxidative stress, inflammation, and endocrine disruption. Natural antioxidants, mainly polyphenols, carotenoids, and vitamins, have been shown to mitigate heavy metal-induced reproductive toxicity potentially. In this review, accumulated evidences on the influences of four non-essential heavy metals As, Cd, Pb, and Hg on both males and females reproductive system were established. The purpose of this review is to explore the potential mechanisms of the effects of heavy metals on reproductive function and point out the potential biomarkers of natural antioxidants interventions toward heavy metal-induced reproductive toxicity. Notably, increasing evidence proven that the regulations of hypothalamic-pituitary-gonadal axis, Nrf2, MAPK, or NF-κB pathways are the important mechanisms for the amelioration of heavy metal induced reproductive toxicity by natural antioxidants. It also provided a promising guidance for prevention and management of heavy metal-induced reproductive toxicity.

The consequence and mechanism of dietary flavonoids on androgen profiles and disorders amelioration.

Androgen is a kind of steroid hormone that plays a vital role in reproductive system and homeostasis of the body. Disrupted androgen balance serves as the causal contributor to a series of physiological disorders and even diseases. Flavonoids, as an extremely frequent family of natural polyphenols, exist widely in plants and foods and have received great attention when considering their inevitable consumption and estrogen-like effects. Mounting evidence illustrates that flavonoids have a propensity to interfere with androgen synthesis and metabolism, and also have a designated improvement effect on androgen disorders. Therefore, flavonoids were divided into six subclasses based on the structural feature in this paper, and the literature about their effects on androgens published in the past ten years was summarized. It could be concluded that flavonoids have the potential to regulate androgen levels and biological effects, mainly by interfering with the hypothalamic-pituitary-gonadal axis, androgen synthesis and metabolism, androgen binding with its receptors and membrane receptors, and antioxidant effects. The faced challenges about androgen regulation by flavonoids masterly include target mechanism exploration, individual heterogeneity, food matrixes interaction, and lack of clinical study. This review also provides a scientific basis for nutritional intervention using flavonoids to improve androgen disorder symptoms.

Host genetics and gut microbiota jointly regulate blood biochemical indicators in chickens.

Blood biochemical indicators play a crucial role in assessing an individual's overall health status and metabolic function. In this study, we measured five blood biochemical indicators, including total cholesterol (CHOL), low-density lipoprotein cholesterol (LDL-CH), triglycerides (TG), high-density lipoprotein cholesterol (HDL-CH), and blood glucose (BG), as well as 19 growth traits of 206 male chickens. By integrating host whole-genome information and 16S rRNA sequencing of the duodenum, jejunum, ileum, cecum, and feces microbiota, we assessed the contributions of host genetics and gut microbiota to blood biochemical indicators and their interrelationships. Our results demonstrated significant negative phenotypic and genetic correlations (r = - 0.20 ~ - 0.67) between CHOL and LDL-CH with growth traits such as body weight, abdominal fat content, muscle content, and shin circumference. The results of heritability and microbiability indicated that blood biochemical indicators were jointly regulated by host genetics and gut microbiota. Notably, the heritability of HDL-CH was estimated to be 0.24, while the jejunal microbiability for BG and TG reached 0.45 and 0.23. Furthermore, by conducting genome-wide association study (GWAS) with the single-nucleotide polymorphism (SNPs), insertion/deletion (indels), and structural variation (SV), we identified RAP2C, member of the RAS oncogene family (RAP2C), dedicator of cytokinesis 11 (DOCK11), neurotensin (NTS) and BOP1 ribosomal biogenesis factor (BOP1) as regulators of HDL-CH, and glycerophosphodiester phosphodiesterase domain containing 5 (GDPD5), dihydrodiol dehydrogenase (DHDH), and potassium voltage-gated channel interacting protein 1 (KCNIP1) as candidate genes of BG. Moreover, our findings suggest that cecal RF39 and Clostridia_UCG_014 may be linked to the regulation of CHOL, and jejunal Streptococcaceae may be involved in the regulation of TG. Additionally, microbial GWAS results indicated that the presence of gut microbiota was under host genetic regulation. Our findings provide valuable insights into the complex interaction between host genetics and microbiota in shaping the blood biochemical profile of chickens. KEY POINTS: • Multiple candidate genes were identified for the regulation of CHOL, HDL-CH, and BG. • RF39, Clostridia_UCG_014, and Streptococcaceae were implicated in CHOL and TG modulation. • The composition of gut microbiota is influenced by host genetics.

Anthocyanin supplement as a dietary strategy in cancer prevention and management: A comprehensive review.

Anthocyanins are natural pigments proven to be beneficial in the vast majority of health problems with no side effects. In this review, the latest progress on the cancer prevention and management of anthocyanins in treating cancers ranked in the top 5 of incidence and mortality was summarized, and the interaction and corresponding mechanisms were established based on a systematic review of electronic libraries. Several studies have revealed that anthocyanins have positive impact on human health with anti-cancer capacity. This review aimed to accumulate the evidence on the anti-cancer effects of anthocyanins, corresponding mechanisms and limitation of anthocyanins on cancer prevention and management. Notably, this review updated the latest studies on cancer prevention and management of anthocyanins and also inputted the future perspectives and the demanding questions for the possible contribution of anthocyanins as anti-cancer adjuvant.

Effects of Bisphenol A on reproductive toxicity and gut microbiota dysbiosis in male rats.

Bisphenol A (BPA) is an environmental endocrine disruptor. Recent studies have shown an association between decreased spermatogenesis and gut microbiota alteration. However, the potential associations and mechanisms of BPA exposure on spermatogenesis, hormone production, and gut microbiota remain unknown. This study aims to investigate BPA-induced male reproductive toxicity and the potential link with gut microbiota dysbiosis. Male Sprague Dawley rats were exposed to BPA at different doses by oral gavage for thirty consecutive days. The extent of testicular damage was evaluated by basic parameters of body weight and hematoxylin-eosin (H&E) staining. Next, we determined the mRNA levels and protein levels of apoptosis, histone-related factors, and mammalian target of rapamycin (mTOR) pathway in testes. Finally, 16 S rDNA sequencing was used to analyze gut microbiota composition after BPA exposure. BPA exposure damaged testicular histology, significantly decreased sperm count, and increased sperm abnormalities. In addition, BPA exposure caused oxidative stress and cell apoptosis in testes. The levels of histone (H2A, H3) were significantly increased, while ubiquitin histone H2A (ub-H2A) and ubiquitin histone H2B (ub-H2B) were markedly reduced. Furthermore, BPA activated the PI3K and AKT expression, but the protein expressions of mTOR and 4EBP1 in testes were inhibited significantly. Additionally, the relative abundance of class Gammaproteobacteria, and order Betaproteobacteriales was significantly higher when treated with a high dose of BPA compared to the control group, which was negatively correlated with testosterone level. This study highlights the relationship between BPA-induced reproductive toxicity and gut microbiota disorder and provides new insights into the prevention and treatment of BPA-induced reproductive damage.

Exposure to Bisphenol A Caused Hepatoxicity and Intestinal Flora Disorder in Rats.

Bisphenol A (BPA) is a globally utilized industrial chemical and is commonly used as a monomer of polycarbonate plastics and epoxy resins. Recent research reveals that BPA could cause potential adverse biological effects and liver dysfunction. However, the underlying mechanisms of BPA-induced hepatoxicity and gut dysbiosis remain unclear and deserve further study. In this study, male Sprague Dawley rats were exposed to different doses (0, 30, 90, and 270 mg/kg bw) of BPA by gavage for 30 days. The results showed that the high dose of BPA decreased superoxide dismutase (SOD), glutathione (GSH), and increased malondialdehyde (MDA) levels. Moreover, a high dose of BPA caused a significant increase in serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), total cholesterol (TC), and low-density lipoprotein cholesterol (LDL-C), while high-density lipoprotein cholesterol (HDL-C) was significantly decreased in BPA-treated rats. The gene expression of PGC-1α and Nrf1 were decreased in the liver of high doses of BPA-administrated rats, as well as the protein levels of SIRT1, PGC-1α, Nrf2, and TFAM. However, the protein expression of IL-1ß was significantly increased in BPA-treated rats. In addition, BPA weakened the mitochondrial function of hepatocytes and promoted cell apoptosis in the liver by up-regulating the protein levels of Bax, cleaved-Caspase3, and cleaved-PARP1 while down-regulating the Bcl-2 in the liver. More importantly, a high dose of BPA caused a dramatic change in microbiota structure, as characterized at the genus level by increasing the ratio of Firmicutes to Bacteroidetes (F/B), and the relative abundance of Proteobacteria in feces, while decreasing the relative abundance of Prevotella_9 and Ruminococcaceae_UCG-014, which is positively correlated with the content of short-chain fatty acids (SCFAs). In summary, our data indicated that BPA exposure caused hepatoxicity through apoptosis and the SIRT1/PGC-1α pathway. BPA-induced intestinal flora and SCFA changes may be associated with hepatic damage. The results of this study provide a new sight for the understanding of BPA-induced hepatoxicity.

miR-1470 regulates cell proliferation and apoptosis by targeting ALX4 in hepatocellular carcinoma.

BACKGROUND: Hepatocellular carcinoma (HCC) is one of the most common malignant tumors worldwide. MicroRNAs (miRNAs) have been proven to play essential roles in different cancers, including HCC. The current study was mainly focused on the role of miR-1470 in HCC progression. METHODS: Quantitative real-time PCR (qRT-PCR) was performed to detect the expression levels of miR-1470 and Aristaless-like homeobox-4 (ALX4). The CCK-8 and EdU assays were used to examine cell proliferation. Flow cytometric analysis was used to elucidate the cell cycle and cell apoptosis. A xenograft tumor assay was carried out to verify the effect of miR-1470 on tumor formation in vivo. RESULTS: According to the qRT-PCR assay, miR-1470 was proven to be overexpressed in HCC. As shown by the CCK-8 assay, EdU assay and flow cytometric analysis, miR-1470 overexpression promoted cell proliferation and inhibited cell apoptosis. ALX4 was proven via a dual luciferase reporter assay to be a downstream target gene of miR-1470. ALX4 was downregulated in HCC. The results of a rescue assay revealed that miR-1470 had an oncogenic role in HCC by regulating ALX4. CONCLUSION: miR-1470 exhibits an oncogenic role in HCC by targeting ALX4. The data from our study may provide novel insight for the identification of new biomarkers and treatment strategies for HCC.

LncRNA ST8SIA6-AS1 promotes hepatocellular carcinoma cell proliferation and resistance to apoptosis by targeting miR-4656/HDAC11 axis.

BACKGROUND: Dysregulation of long non-coding RNAs (lncRNAs) results in development of human diseases including hepatocellular carcinoma (HCC). Although several HCC related lncRNAs have been reported, the biological functions of many lncRNAs during the development of HCC remains unknown. METHODS: The expression of ST8SIA6-AS1 was studied by realtime PCR (RT-qPCR) and bioinformatic analysis. The biological functions of ST8SIA6-AS1 was examined by CCK-8 assay and flow cytometry analysis. The target of ST8SIA6-AS1 was analyzed by bioinformatic analysis and validated by dual luciferase reporter assay, western blotting and RT-qPCR. RESULTS: In this study we demonstrated that ST8SIA6-AS1 was an upregulated lncRNA in hepatocellular carcinoma. SiRNA-mediated knockdown of ST8SIA6-AS1 repressed cell proliferation and induced cell apoptosis in HCC cells. Bioinformatic analysis and RT-qPCR further showed that ST8SIA6-AS1 mainly located in cytoplasm. Dual luciferase reporter assay further revealed that ST8SIA6-AS1 interacted with miR-4656 in HCC cells. In addition, HDAC11 was identified as a target gene in HCC cells and ST8SIA6-AS1 could upregulate HDAC11 via sponging miR-4656. Transfection of recombinant HDAC11 partially rescued the inhibition of cell proliferation and increase of cell apoptosis inducing by knockdown of ST8SIA6-AS1. CONCLUSION: In conclusion, our findings suggested that ST8SIA6-AS1 was a novel upregulated lncRNA in HCC and could facilitate cell proliferation and resistance to cell apoptosis via sponging miR-4656 and elevation of HDAC11, which might be a promising biomarker for patients with HCC.

Bioactive compounds from Cudrania tricuspidata: A natural anticancer source.

The tumor is becoming a critical threat to our lives in these years. Searching for antitumor substances from natural products is a great interest of scientists. Cudrania tricuspidata (C. tricuspidata) is a regional plant containing 158 flavonoids and 99 xanthones, and others ingredients with favorable bioactivity. This review comprehensively analyzes the antitumor compounds from C. tricuspidata against different tumors, and 78 flavonoids plus xanthones are considered as underlying antineoplastic. Importantly, the structure of preylation groups is the primary source of antitumor activity among 45 flavonoids plus xanthones, which could be a direction of structural modification for a better antitumor ability. Additionally, the fruits are also preferable sources of antitumor compounds compared to the roots and barks due to the abundant isoflavones and sustainability. However, many studies only focused on the cells viability inhibition of the compounds, the underlying molecular mechanisms, and the intracellular targets remain ambiguous. In conclusion, C. tricuspidata has a great potential for anti-tumor prevention or therapy, but more attention should be paid to deeper research in vitro and in vivo models.

First report of a novel partitivirus from the phytopathogenic fungus Fusarium cerealis in China.

To our knowledge, no mycoviruses have been reported in Fusarium cerealis. Here, we describe a novel double-stranded RNA (dsRNA) virus, Fusarium cerealis partitivirus 1 (FcPV1), isolated from F. cerealis strain HN30 from Henan Province, China. The FcPV1 genome consists of two dsRNA segments, 1732 bp (dsRNA1) and 1361 bp (dsRNA2) in length, each containing a single open reading frame potentially encoding a 61.0-kDa protein and a 42.0-kDa protein, respectively. dsRNA1 encodes a putative RNA-dependent RNA polymerase (RdRp), while the dsRNA2 product has no significant similarity to any other capsid proteins (CPs) in the GenBank databases other than limited similarity to hypothetical "capsid" proteins of a few partitiviruses. Sequence alignments and phylogenetic analysis showed that FcPV1 is related to members of the newly proposed genus "Zetapartitivirus" in the family Partitiviridae.

Modafinil ameliorated pancreatic injury and inflammation through upregulating SNIP1.

Acute pancreatitis (AP) is the inflammatory response of the exocrine pancreas to various causes. Modafinil has significant anti-inflammation and anti-oxidation effects. No experiment has assessed the effects of modafinil on AP. Thus, the study aims to study the effects of modafinil on AP and its potential mechanism in vivo and vitro. 5% sodium taurocholate was retrograde injected into pancreatic duct to establish AP rat model. The severity of AP was detected by HE staining, serum amylase and lipase levels. The inflammation, oxidative stress and apoptosis were detected separately by ELISA, MDA and SOD kits, tunnel staining and Western blotting in rats. Besides, SNIP1 expression was analyzed by qPCR and Western blotting. In vivo, AR42J cells were stimulated by cerulein and lipopolysaccharide to establish AP cell model. Flow cytometry examined cell apoptosis. After the plasmids silencing SNIP1 were transfected into AP cells, the inhibitory effects of modafinil on inflammation, oxidative stress and apoptosis were significantly reversed. The results indicated that modafinil showed significant curative and therapeutic effects by regulating SNIP1 level.

Sparse Feature Learning of Hyperspectral Imagery via Multiobjective-Based Extreme Learning Machine.

Hyperspectral image (HSI) consists of hundreds of narrow spectral band components with rich spectral and spatial information. Extreme Learning Machine (ELM) has been widely used for HSI analysis. However, the classical ELM is difficult to use for sparse feature leaning due to its randomly generated hidden layer. In this paper, we propose a novel unsupervised sparse feature learning approach, called Evolutionary Multiobjective-based ELM (EMO-ELM), and apply it to HSI feature extraction. Specifically, we represent the task of constructing the ELM Autoencoder (ELM-AE) as a multiobjective optimization problem that takes the sparsity of hidden layer outputs and the reconstruction error as two conflicting objectives. Then, we adopt an Evolutionary Multiobjective Optimization (EMO) method to solve the two objectives, simultaneously. To find the best solution from the Pareto solution set and construct the best trade-off feature extractor, a curvature-based method is proposed to focus on the knee area of the Pareto solutions. Benefited from the EMO, the proposed EMO-ELM is less prone to fall into a local minimum and has fewer trainable parameters than gradient-based AEs. Experiments on two real HSIs demonstrate that the features learned by EMO-ELM not only preserve better sparsity but also achieve superior separability than many existing feature learning methods.

The target cells of anthocyanins in metabolic syndrome.

Metabolic syndrome develops to several related chronic diseases, such as obesity, cardiovascular disease, hypertension, diabetes, and fatty liver disease. Diseases are outcomes of various cells dysfunction, which are especially acting with a network in metabolic syndrome. Anthocyanins are natural edible pigments widely existed in dark-colored fruits, vegetables, and grains. Epidemiological investigation and nutritional intervention of anthocyanins have exhibited broad-spectrum biological effects that they can benefit patients with metabolic syndrome related chronic diseases. Whereas the underlying mechanisms and the effects of anthocyanins on critical cells in chronic metabolic diseases are complex and elusive. Therefore, this review summarizes the studies about the effects of anthocyanins on various metabolism related chronic diseases, and mainly focuses on the effects and underlying molecular mechanisms on critical cells. We confirmed that anthocyanins are efficient on adipocytes, endothelial cells, inflammatory cells, hepatocytes, intestinal cells and gut microbiota, but lack of evidence on platelets, skeletal muscle cells, hepatic stellate cells and pancreatic beta cells. Additionally, we discussed the structure-function relationship of anthocyanins and the metabolites. This review summarizes the development of studies on anthocyanins with its target cells in metabolic syndrome, and discusses the unclear aspects of the anthocyanins research work, which is necessary for the future clinical application.

MNX1 promotes cell proliferation and activates Wnt/ß-catenin signaling in colorectal cancer.

Aberrant Wnt/ß-catenin signaling is a characteristic feature of colorectal cancer (CRC), therefore, understanding the underlying mechanisms of aberrant Wnt/ß-catenin signaling will improve the treatment outcome of CRC. Expression of MNX1 in paired fresh CRC tissues and corresponding adjacent normal tissues were examined by qPCR and Western blotting. The levels of MNX1 in paraffin-embedded CRC specimens were detected by immunohistochemistry (IHC). The role of MNX1 in growth and proliferation of CRC cells was evaluated by MTT and colony formation assay. Luciferase reporter analysis and western blotting were carried out to explore the influence of MNX1 on Wnt/ß-catenin signaling. The results showed that expression of MNX1 is markedly upregulated in CRC tissues and positively correlated with level of Ki67, and overexpression of MNX1 significantly promotes the proliferation of CRC cells. Further study showed that ectopic expression of MNX1 activates the Wnt/ß-catenin signaling and upregulates the expression of c-Myc and CCND1, the downstream genes of Wnt/ß-catenin signaling. Therefore, MNX1 plays an indispensable role in promoting of human CRC progression and may represent a novel therapeutic target for CRC.

Comparison on the Efficacy of Three Duct Closure Methods after Laparoscopic Common Bile Duct Exploration for Choledocholithiasis.

BACKGROUND Laparoscopic common bile duct exploration (LCBDE) is currently the best approach for complex cases of choledocholithiasis or the cases of endoscopic retrograde cholangiopancreatography (ERCP) failure. Nevertheless, there is no clear consensus on the optimal duct closure method after LCBDE. The purpose of this study was to evaluate the efficacy of 3 duct closure methods after LCBDE for choledocholithiasis. MATERIAL AND METHODS In this analysis, 189 patients with choledocholithiasis underwent LCBDE between June 2014 and December 2018. According to different duct closure methods, these patients were divided into T-tube drainage (TTD) group (n=66), common suture group (n=64) and barbed suture group (n=59). The operation time, suturing time, amount of intraoperative bleeding, tube-carried time, length of stay (LOS), hospitalization costs, pre- and post-operative common bile duct (CBD) diameters were all compared among the 3 groups. Six months after discharge, the incidence of complications and recurrent stones was observed. RESULTS The operation time, suturing time, and amount of intraoperative bleeding in barbed suture group were both significantly less than those in the common suture group and the TTD group (P<0.01). When compared with the TTD group, the suturing time, tube-carried time, and LOS were decreased markedly in the common suture group and the barbed suture group (P<0.01). The post-operative CBD diameters in the 3 groups were all significantly larger than the pre-operative CBD diameters (P<0.01). There was no statistical significance among the 3 groups regarding the incidence of complications and recurrent stones (P>0.05). CONCLUSIONS Barbed suture shortened the suturing time, operation time, tube-carried time, and LOS, and lessened the amount of intraoperative bleeding in patients with choledocholithiasis after LCBDE. It was more effective than the common suture and TTD.

Spectral-Spatial Feature Extraction of Hyperspectral Images Based on Propagation Filter.

Recently, image-filtering based hyperspectral image (HSI) feature extraction has been widely studied. However, due to limited spatial resolution and feature distribution complexity, the problems of cross-region mixing after filtering and spectral discriminative reduction still remain. To address these issues, this paper proposes a spectral-spatial propagation filter (PF) based HSI feature extraction method that can effectively address the above problems. The dimensionality/band of an HSI is typically high; therefore, principal component analysis (PCA) is first used to reduce the HSI dimensionality. Then, the principal components of the HSI are filtered with the PF. When cross-region mixture occurs in the image, the filter template reduces the weight assignments of the cross-region mixed pixels to handle the issue of cross-region mixed pixels simply and effectively. To validate the effectiveness of the proposed method, experiments are carried out on three common HSIs using support vector machine (SVM) classifiers with features learned by the PF. The experimental results demonstrate that the proposed method effectively extracts the spectral-spatial features of HSIs and significantly improves the accuracy of HSI classification.

Interleukin-17A exacerbates high-fat diet-induced hepatic steatosis by inhibiting fatty acid ß-oxidation.

There is a growing body of evidence that the interleukin-17A (IL-17A) signaling pathway contributes to the pathogenesis of nonalcoholic fatty liver disease (NAFLD). However, the mechanism by which IL-17A signaling induces hepatocyte injury is unclear. The aim of the present study was to investigate the significance of the IL-17A axis in NAFLD and to explore the role of IL-17A in high-fat diet (HFD)-induced NAFLD in C57BL/6 mice and oleic acid (OA)-induced lipid accumulation in hepatocytes. Firstly, Consistent upregulation of IL-17A was observed in the HFD-induced steatosis mice but not the normal chow-fed control mice. Administration of IL-17A impaired liver function, aggravated hepatic lipid accumulation by inhibiting fatty acid oxidation in the HFD mice. Conversely, inhibition of IL-17A using an anti-IL-17A monoclonal antibody (mAb) significantly attenuated HFD-induced liver injury. Furthermore, IL-17A accelerated hepatic steatosis through activation of the JNK-PPARα pathway in the HFD mice and OA-preloaded hepatocytes. CONCLUSION: The present study demonstrated that a high fat diet induces IL-17A expression, which exacerbates the progression of NAFLD by inhibiting fatty acid ß-oxidation and promoting the accumulation of triglycerides (TG).

Cyanidin-3-O-glucoside and its derivative vitisin A alleviate androgenetic alopecia by exerting anti-androgen effect and inhibiting dermal papilla cell apoptosis.

Androgenetic alopecia (AGA), one of the most common forms of hair loss, lacks satisfactory treatment methods in modern society. This study employed an experimental design combining in vitro and in vivo approaches to explore the effects of Cyanidin-3-O-glucoside (C3G) and Carboxypyranocyanidin-3-O-glucoside (Vitisin A) on AGA. In human dermal papilla cells (HDPCs), both anthocyanins demonstrated inhibitory effects on androgen receptors, significantly reduced dihydrotestosterone (DHT) induced apoptosis of HDPCs, and regulated the secretion of Fibroblast growth factor 7 and Transforming growth factor beta 1. In vitro transdermal experiment revealed that both C3G and Vitisin A could penetrate mice skin, aided by the application of cream. Furthermore, in vivo experiments with mice indicated that application of C3G or Vitisin A cream effectively improved hair follicles miniaturization, regression, and apoptosis caused by DHT. The repression of Wnt10b and ß-catenin expression induced by DHT was prevented by C3G and Vitisin A in both cell and mouse model. Consequently, these findings suggest that C3G and Vitisin A could be considered as alternative methods for alleviating AGA.

Variations in seminal microbiota and their functional implications in chickens adapted to high-altitude environments.

Seminal fluid, once believed to be sterile, is now recognized as constituting a complex and dynamic environment inhabited by a diverse community of micro-organisms. However, research on the seminal microbiota in chickens is limited, and microbiota variations among different chicken breeds remain largely unexplored. In this study, we collected semen samples from Beijing You Chicken (BYC) and Tibetan Chicken (TC) and explored the characteristics of the microbiota using 16S rRNA gene sequencing. Additionally, we collected cloacal samples from the TC to control for environmental contamination. The results revealed that the microbial communities in the semen were significantly different from those in the cloaca. Firmicutes and Actinobacteriota were the predominant phyla in BYC and TC semen, respectively, with Lactobacillus and Phyllobacterium being the dominant genera in each group. Additionally, the seminal microbiota of BYC exhibited greater richness and evenness than that of TC. Principal coordinate analysis (PCoA) indicated significant intergroup differences between the seminal microbiotas of BYC and TC. Subsequently, by combining linear discriminant analysis effect size and random forest analyses, we identified Lactobacillus as the predominant microorganism in BYC semen, whereas Phyllobacterium dominated in TC semen. Furthermore, co-occurrence network analysis revealed a more intricate network in the BYC group than in the TC group. Additionally, unique microbial functional characteristics were observed in each breed, with TC exhibiting metabolic features potentially associated with their ability to adapt to high-altitude environments. The results of this study emphasized the unique microbiota present in chicken semen, which may be influenced by genetics and evolutionary history. Significant variations were observed between low-altitude and high-altitude breeds, highlighting the breed-specific implications of the seminal microbiota for reproduction and high-altitude adaptation.