The promising stability of carboxylpyranocyanidin-3-O-glucoside during food processing and simulated digestion and its bioavailability research.

BACKGROUND: Pyranoanthocyanins are stable anthocyanin derivatives. Carboxylpyranoanthocyanin is one of the simplest pyranoanthocyanin, among which the production of carboxylpyranocyanidin-3-O-glucoside (crboxyl-pycy-3-gluc) is most feasible as a result of the abundance of its reactant, cyanidin-3-O-glucoside (Cy-3-gluc). RESULTS: In the present study, carboxyl-pycy-3-gluc was synthesized and its stability during processing and after ingestion as well as its bioavailability in vivo were comprehensively evaluated. Our results indicated that the color of carboxyl-pycy-3-gluc remained more stable compared to Cy-3-gluc when facing the large-span pH variation. The high retention of anthocyanin symbolized the superb stability under thermal processing, sulfur dioxide bleaching and ultrasonic treatment of carboxyl-pycy-3-gluc. Because of the stability under the alkaline condition, carboxyl-pycy-3-gluc is more stable after oral-gastrointestinal digestion. After in vitro gut microbiota fermentation, the retention of carboxyl-pycy-3-gluc was significantly higher than that of Cy-3-gluc. The larger molecular size made absorption of carboxyl-pycy-3-gluc into blood more difficult than its precursor. CONCLUSION: The present study demonstrated the promising stability of carboxyl-pycy-3-gluc during food processing and after digestion, confirming the potential of carboxyl-pycy-3-gluc as a colorant. © 2023 Society of Chemical Industry.

Vitisin A, as a Type of Pyranoanthocyanin, Suppresses Inflammation by Restricting Hematopoietic Stem Cell Differentiation toward Monocytes in Bone Marrow.

Hematopoietic stem and progenitor cells (HSPCs) could be differentiated into mature myeloid and lymphoid cells, maintaining the requirements of immune cells. Atherosclerosis and ulcerative colitis (UC) drive HSPC homeostasis destruction, which triggers expansive HSPC proliferation and Ly6Chi monocyte production, contributing to aggravated inflammation. Vitisin A belongs to the anthocyanin derivatives with excellent stability and bioactivity in vitro. However, there is no report about the anti-inflammation of Vitisin A via reprogramming HSPC differentiation toward monocytes. In this study, we found that Vitisin A presents anti-inflammatory ability during the development of atherosclerosis and UC by depressing Ly6Chi monocyte production from bone marrow. This performance depended on restricted HSPC differentiation, which suggested that Vitisin A participated in monocyte generation and carried out the immunomodulation. Together, Vitisin A ameliorates inflammation during atherosclerosis and UC via the suppressed differentiation of HSPCs toward monocytes, which could be considered an ideal functional component with immunomodulatory effects.

Induction of reproductive injury by bisphenol A and the protective effects of cyanidin-3-O-glucoside and protocatechuic acid in rats.

Bisphenol A (BPA) has attracted growing attention as a well-known environmental pollutant due to its high risk of male reproductive toxicity. In this study, transcriptomics profiling combined with metabolomic techniques was applied to explore the intervention effects of BPA-induced male reproductive toxicity. We demonstrated that cyanidin-3-O-glucoside (C3G) and its main metabolite protocatechuic acid (PCA) significantly increased testosterone and luteinizing hormone (LH) levels in the serum of rats, and improved sperm quality. Furthermore, we identified and screened differentially expressed genes (DEGs) and metabolites (DMs) that functionally enriched in the steroidogenesis-related pathways. Next, the validated results found that C3G and PCA significantly up-regulated the gene expressions of Star, Cyp11a1, Cyp17a1, Cyp19a1, Cyp7a1, Hsd3b1, Hsd3b2, Hsd17b3, Scrab1, and Ass1 in testicular. In Leydig cells, C3G and PCA dramatically alleviated apoptosis, ROS accumulation, and cell cycle arrest caused by BPA. In addition, molecular docking and simulation results implied that C3G and PCA competitively with BPA bind to the estrogen receptors α and ß (ERα and ERß) and shared common key amino acids. The main interaction modes between small molecules and estrogen receptors included π-π stacking, salt bridges, hydrogen bonds, and hydrophobic interactions. Therefore, our study sheds light on C3G and PCA supplementation can protect male reproduction from BPA-induced injury.

Cyanidin-3-O-glucoside and protocatechuic acid alleviate heat stress-induced testicular damage.

Testicular hyperthermia induced by unhealthy living habits and pathological or occupational factors can cause spermatogenic dysfunction with an outcome of sub-fertility or even infertility. Cyanidin-3-O-glucoside (C3G) is the most typical anthocyanin in foods that has been recognized as an antioxidant with promising protection for male reproduction. However, its specific effect against testicular hyperthermia and the mechanisms involving its primary gastrointestinal metabolite protocatechuic acid (PCA) are still unexplored. In the present study, testicular hyperthermia in mice was established by employing a single hot water bath at 43 °C for 30 min. C3G and PCA were intragastrically given to investigate their prevention ability against heat stress-induced testicular damage. It was found that C3G and PCA restored the external diameter and thickness, and alleviated atrophy and vacuolation of seminiferous tubules. Simultaneously, C3G and PCA enhanced testicular heat stress tolerance through reducing superfluous eIF2α phosphorylation and stress granule formation. C3G and PCA effectively improved the testicular antioxidant system and regulated the IRE1α-XBP1 pathway, contributing to mitigatory spermatogenesis dysfunction and testicular damage. This finding revealed that anthocyanins were the novel compounds for alleviating testicular damage, and provided a reliable theoretical basis for improving male fertility disturbed by heat stress.

Untargeted Lipidomics Revealed the Protective Effects of Cyanidin-3-O-glucoside on Bisphenol A-Induced Liver Lipid Metabolism Disorder in Rats.

Bisphenol A (BPA) is an estrogenic endocrine disruptor that induces metabolic disorders. Cyanidin-3-O-glucoside (C3G) has multiple functional activities and is the most abundant anthocyanin belonging to the flavonoid subgroup. This study aimed to investigate the protective effect of C3G on BPA-induced liver lipid metabolism disorder and explore its mechanism via lipidomics analysis. The results showed that C3G supplementation significantly ameliorated the serum levels of low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, total cholesterol, triacylglycerols (TG), and alanine and aspartate aminotransferase (ALT and AST). Furthermore, liver lipidomics indicated that C3G effectively facilitated the recovery of differential lipid metabolites, including TGs, phosphatidylethanolamines, phosphatidylcholines, lysophosphatidylcholines, phosphatidylinositol, cholesteryl esters, and phosphatidylserine, and reversed the levels of hepatic lipid synthesis-related genes. Our results suggest that C3G has an effective regulatory effect on BPA-induced disorders of lipid metabolism.

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.

Color Stability Enhancement and Antioxidation Improvement of Sanhua Plum Wine under Circulating Ultrasound.

Anthocyanins contribute to the attractive color of fruit wine, and their excessive degradation is deleterious to quality, especially for wine with an inherently low anthocyanin content, such as Sanhua plum wine. Ultrasonic treatment is well recognized for wine color maintenance. In the present study, fresh Sanhua plum wine was ultrasonic-treated and aged in barrels for three months. Our results demonstrate that ultrasonic treatment at 28 and 40 kHz improves color performance, as expressed by an increase in a*, b*, and C* values and color intensity, which is highly related to copigmentation. This successful conservation was attributed to the inactivation of polyphenol oxidase and the corresponding reduction in anthocyanin degradation. Finally, the increased antioxidative ability was verified due to the hydrogen donating ability of the surviving anthocyanins. This study indicates the reliability of ultrasonic treatment for providing superior colorfastness during Sanhua plum wine aging, which is also of great potential in processing different fruit wines.

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.

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.

A comprehensive review on innovative and advanced stabilization approaches of anthocyanin by modifying structure and controlling environmental factors.

Anthocyanins are pigments abundant in fruits and vegetables, and commonly applied in foods due to attractive colour and health-promoting benefits. However, instability of anthocyanins leads to their easy degradation, reduced bioactivity, and colour fading in food processing, limiting their application and causing economic losses. Stability of anthocyanins depends on their own structures and environmental factors. For structural factors, modification including copigmentation, acylation and biosynthesis is a potential solution to increase anthocyanin stability due to forming stable structures. With regard to environmental factors, encapsulation such as microencapsulation, liposome and nanoparticles has been shown effectively to enhance the stability. We proposed the potential challenges and perspectives for the diversification of anthocyanin-rich products for food application, particularly, introduction of hazards, technical limitations, interaction with other ingredients in food system and exploration of pyranoanthocyanins. The integrated strategies are warranted for improving anthocyanin stabilization for promoting their further application in food industry.

Chronic oral exposure to cadmium causes liver inflammation by NLRP3 inflammasome activation in pubertal mice.

Cadmium (Cd) is a potentially toxic trace element frequently existed in foods, water, and air, threatening liver function from its continuous bioaccumulation and induction of oxidative stress and inflammation. However, the hepatotoxicity of Cd during puberty remains unclear. In this study, pubertal mice were given cadmium chloride at a dose of 5.0 mg/kg·bw by gavage, and the liver damage was investigated at different treatment points of 10, 20, and 30 days. After Cd exposure, there is an obvious inflammatory hepatocyte infiltration accompanied by more apoptotic cells at 20 days and an increase in alanine aminotransferases and aspartate aminotransferases in circulation at 30 days. Additionally, the soaring TNF-α and MCP-1 were found in liver, and the mRNA expression of pro-inflammatory cytokines (IL-1α, IL-1ß, and IL-18) and anti-inflammatory cytokines (TGF-ß, IL-10, and IL-13) were both significantly upregulated. Moreover, the activated M1 and M2 macrophages were confirmed in charge of these cytokines release. Most importantly, the data validated a pivotal role of NOD-like receptor pyrin domain containing 3 (NLRP3) inflammasome in Cd-induced inflammation in liver at puberty. Collectively, our results suggested that low-dose Cd oral exposure can cause liver inflammation via activation of NLRP3 inflammasome and give rise to severe liver injury at puberty.

Novel reversibly switchable wettability of superhydrophobic-superhydrophilic surfaces induced by charge injection and heating.

Reversibly switching wettability between superhydrophobicity and superhydrophilicity has attracted widespread interest because of its important applications. In this work, we propose a reversible superhydrophobic-superhydrophilic conversion induced by charge injection and heating. Different from the conventional electrowetting phenomenon caused by the accumulation of solid-liquid interfacial charges, we discovered a phenomenon where charge injection and accumulation at the solid surface results in a sharp increase in wettability. The wettability of a sprayed SiO2 nanoparticle coating on a glass slide was shown to change from superhydrophobic to superhydrophilic by charge injection and heating, and the superhydrophobicity was restored by heating, verifying a reversible superhydrophobic-superhydrophilic conversion. The influence of voltage, temperature, and time on the coating wettability and its durability under reversible conversion have been studied.