Rapid evaluation of the quality of Smilax glabra Roxb. using QADS based on FT-NIR combined with multiple intelligent algorithms.

Smilax glabra Roxb. (SGR) is known for its high nutritional and therapeutic value. However, the frequent appearance of counterfeit products causes confusion and inconsistent quality among SGR varieties. Herein, this study collected the proportion of SGR adulteration and used high-performance liquid chromatography (HPLC) to measure the astilbin content of SGR. Then Fourier-transform near-infrared (FT-NIR) technology, combined with multivariate intelligent algorithms, was used to establish partial least squares regression quantitative models for detecting SGR adulteration and measuring astilbin content, respectively. The method conducted a quantitative analysis of dual indicators through single-spectrum data acquisition (QADS) to comprehensively evaluate the authenticity and superiority of SGR. The coefficients of determination (R2) for both the calibration and prediction sets exceeded 0.96, which successfully leverages FT-NIR combined with multivariate intelligent algorithms to considerably enhance the accuracy and reliability of quantitative models. Overall, this research holds substantial value in the comprehensive quality evaluation in functional health foods.

Astilbin inhibited neutrophil extracellular traps in gouty arthritis through suppression of purinergic P2Y6 receptor.

BACKGROUND: Gouty arthritis (GA), a common inflammatory condition triggered by monosodium urate crystal accumulation, often necessitates safer treatment alternatives due to the limitations of current therapies. Astilbin, a flavonoid from Smilax glabra Roxb, has demonstrated potential in traditional Chinese medicine for its anti-inflammatory properties. However, the anti-GA effect and its underlying mechanism have not been fully elucidated. PURPOSE: This study aimed to investigate the therapeutic potential of astilbin in GA, focusing on its effects on neutrophil extracellular traps (NETs), as well as the potential molecular target of GA both in vitro and in vivo. STUDY DESIGN: Firstly, astilbin inhibited the citrullinated histone H3 (Cit h3) protein levels and reduced the NETs formation in neutrophils stimulated by monosodium urate (MSU). Secondly, we wondered the effect of astilbin on migration of neutrophils and dimethyl-sulfoxide (DMSO)-differentiated HL-60 (dHL-60) cells under the stimulation of MSU. Then, the effect of astilbin on suppressing NETs through purinergic P2Y6 receptor (P2Y6R) and Interlukin-8 (IL-8)/ CXC chemokine receptor 2 (CXCR2) pathway was investigated. Also, the relationship between P2Y6R and IL-8/CXCR2 was explored in dHL-60 cells under stimulation of MSU. Finally, we testified the effect of astilbin on reducing NETs in GA through suppressing P2Y6R and then down-regulating IL-8/CXCR2 pathway. METHODS: MSU was used to induce NETs in neutrophils and dHL-60 cells. Real-time formation of NETs and migration of neutrophils were monitored by cell living imaging with or without MSU. Then, the effect of astilbin on NETs formation, P2Y6R and IL-8/CXCR2 pathway were detected by immunofluorescence (IF) and western blotting. P2Y6R knockdown dHL-60 cells were established by small interfering RNA to investigate the association between P2Y6R and IL-8/CXCR2 pathway. Also, plasmid of P2Y6R was used to overexpress P2Y6R in dHL-60 cells, which was employed to explore the role of P2Y6R in astilbin inhibiting NETs. Within the conditions of knockdown and overexpression of P2Y6R, migration and NETs formation were assessed by transmigration assay and IF staining, respectively. In vivo, MSU-induced GA mice model was established to assess the effect of astilbin on inflammation by haematoxylin-eosin and ELISA. Additionally, the effects of astilbin on neutrophils infiltration, NETs, P2Y6R and IL-8/CXCR2 pathway were analyzed by IF, ELISA, immunohistochemistry (IHC) and western blotting. RESULTS: Under MSU stimulation, astilbin significantly suppressed the level of Cit h3 and NETs formation including the fluorescent expressions of Cit h3, neutrophils elastase, myeloperoxidase, and intra/extracellular DNA. Also, results showed that MSU caused NETs release in neutrophils as well as a trend towards recruitment of dHL-60 cells to MSU. Astilbin could markedly decrease expressions of P2Y6R and IL-8/CXCR2 pathway which were upregulated by MSU. By silencing P2Y6R, the expression of IL-8/CXCR2 pathway and migration of dHL-60 cells were inhibited, leading to the suppression of NETs. These findings indicated the upstream role of P2Y6R in the IL-8/CXCR2 pathway. Moreover, overexpression of P2Y6R was evidently inhibited by astilbin, causing a downregulation in IL-8/CXCR2 pathway, migration of dHL-60 cells and NETs formation. These results emphasized that astilbin inhibited the IL-8/CXCR2 pathway primarily through P2Y6R. In vivo, astilbin administration led to marked reductions in ankle swelling, inflammatory infiltration as well as neutrophils infiltration. Expressions of P2Y6R and IL-8/CXCR2 pathway were evidently decreased by astilbin and P2Y6R inhibitor MRS2578 either alone or in combination. Also, astilbin and MRS2578 showed notable effect on reducing MSU-induced NETs formation and IL-8/CXCR2 pathway whether used alone or in combination, parallelly demonstrating that astilbin decreased NETs formation mainly through P2Y6R. CONCLUSION: This study revealed that astilbin suppressed NETs formation via downregulating P2Y6R and subsequently the IL-8/CXCR2 pathway, which evidently mitigated GA induced by MSU. It also highlighted the potential of astilbin as a promising natural therapeutic for GA.

Advances in the chemical constituents, pharmacological activity, and clinical application of Smilacis Glabrae Rhizoma: A review and predictive analysis of quality markers (Q-markers).

Smilacis Glabrae Rhizoma (SGR) is recognized in traditional Chinese medicine for its distinctive therapeutic properties and abundant supply. Its phytochemical profile is diverse, encompassing flavonoids, steroids, saccharides, phenolic glycosides, volatile constituents, organic acids, phenylpropanoids, stilbenoids, among others. Recent pharmacological investigations reveal that SGR possesses a broad spectrum of pharmacological effects with multifaceted clinical applications. This review collates the current knowledge on SGR's chemical composition, pharmacological activities, and its clinical utility. Utilizing network pharmacology and molecular docking approaches, this study provides a preliminary identification of potential quality markers (Q-Markers) within SGR. The findings suggest that compounds such as astilbin, isoengelitin, neoisoastilbin, neoastilbin, astragaloside, diosgenin, resveratrol, stigmasterol, ß-sitosterol, and quercetin in SGR are promising candidates for Q-Markers. While flavonoids are the most extensively studied, there is a pressing need to further explore the active monomeric compounds within SGR. The introduction of Q-Markers is instrumental in developing standardized quality metrics. Specifically, astilbin has been noted for its antitumor, antidiabetic, antihypertensive, anti-hyperuricemic, and hepatoprotective potential, warranting further research for therapeutic applications.

The antagonism mechanism of astilbin against cadmium-induced injury in chicken lungs via Treg/Th1 balance signaling pathway.

The purpose of this study was to investigate the effect of Treg/Th1 imbalance in cadmium-induced lung injury and the potential protective effect of astilbin against cadmium-induced lung injury in chicken. Cadmium exposure significantly decreased T-AOC and GSH-Px levels and SOD activity in the chicken lung tissues. In contrast, it significantly increased the MDA and NO levels. These results indicate that cadmium triggers oxidative stress in lungs. Histopathological analysis revealed that cadmium exposure further induced infiltration of lymphocytes in the chicken lungs, indicating that cadmium causes pulmonary damage. Further analysis revealed that cadmium decreased the expression of IL-4 and IL-10 but increased those of IL-17, Foxp3, TNF-α, and TGF-ß, indicating that the exposure of cadmium induced the imbalance of Treg/Th1. Moreover, cadmium adversely affected chicken lung function by activating the NF-kB pathway and inducing expression of genes downstream to these pathways (COX-2, iNOS), associated with inflammatory injury in the lung tissue. Astilbin reduced cadmium-induced oxidative stress and inflammation in the lungs by increasing antioxidant enzyme activities and restoring Treg/Th1 balance. In conclusion, our results suggest that astilbin treatment alleviated the effects of cadmium-mediated lung injury in chickens by restoring the Treg/Th1 balance.

Mechanism of Smilax china L. in the treatment of intrauterine adhesions based on network pharmacology, molecular docking and experimental validation.

BACKGROUND: Smilax china L. (SCL) is a traditional herbal medicine for the potential treatment of intrauterine adhesion (IUA). However, the mechanisms of action have not yet been determined. In this study, we explored the effects and mechanisms of SCL in IUA by network pharmacology, molecular docking and molecular biology experiments. METHODS: Active ingredients and targets of SCL were acquired from TCMSP and SwissTargetPrediction. IUA-related targets were collected from the GeneCards, DisGeNET, OMIM and TTD databases. A protein‒protein interaction (PPI) network was constructed by Cytoscape 3.9.1 and analysed with CytoHubba and CytoNCA to identify the core targets. The DAVID tool was used for GO and KEGG enrichment analyses. Furthermore, molecular docking was employed to assess the interaction between the compounds and key targets. Finally, the mechanisms and targets of SCL in IUA were verified by cellular experiments and western blot. RESULTS: A total of 196 targets of SCL were identified, among which 93 were related to IUA. Topological and KEGG analyses results identified 15 core targets that were involved in multiple pathways, such as inflammation, apoptosis, and PI3K/AKT signalling pathways. Molecular docking results showed that the active compounds had good binding to the core targets. In vitro experiments showed that astilbin (AST), a major component of SCL, significantly reduced TGF-ß-induced overexpression of fibronectin (FN), activation of the PI3K/AKT signalling pathway and the expression of downstream factors (NF-κB and BCL2) in human endometrial stromal cells, suggesting that AST ameliorates IUA by mediating the PI3K/AKT/NF-κB and BCL2 proteins. CONCLUSIONS: AST, a major component of SCL, may be a potential therapeutic agent for IUA. Moreover, its mechanism is strongly associated with regulation of the PI3K/AKT signalling pathway and the downstream NF-κB and BCL2 proteins. This study will provide new strategies that utilize AST for the treatment of IUA.

Research progress on ethnobotany, phytochemistry, pharmacological action, and applications of Engelhardia roxburghiana Wall: a review.

OBJECTIVES: Engelhardia roxburghiana Wall is a plant of the Juglandaceae family, and its leaves is the main part used as a medicine. It is used to relieve heat and pain, gasification, and dampness. The purpose of this review is to provide a systematic review about the botany, traditional uses, phytochemistry, pharmacology, and toxicology of this plant. KEY FINDINGS: Many compounds have been isolated and identified from the plant, including flavonoids, triterpenoids, steroids, quinones, essential oils, and other types of chemical constituents. Extensive pharmacological activities of the extracts or compounds of E. roxburghiana Wall in vivo and in vitro were mainly confirmed, including anti-cancer, anti-diabetic, anti-inflammatory, and anti-allergic effects. SUMMARY: In this paper, the botany, traditional uses, phytochemistry, and pharmacology of E. roxburghiana Wall were reviewed. In the future, E. roxburghiana Wall needs further study, such as paying more attention to quality control and the utilization on agriculture. In addition, discussing the medicinal components of decoction as well as the toxicity will also contribute to the progress of clinical trial studies.

Lipid Carrier Nanostructured Astilbin Ameliorates Rotenone-Induced Neurodegeneration in Mice Brain via Modulation of GSK3ß-Nrf2 Signaling Pathways.

Astilbin is a flavanonol, found in St John's wort (Hypericum perforatum) and many other plants. It has been demonstrated that astilbin contains anti-inflammatory, antioxidant, and immune-suppressive properties. However, the bioavailability of astilbin remains a question for which drug delivery-based nanoparticles can be utilized. We formulated a nanostructured lipid carrier loaded with astilbin (NLC-AS) and tested its effects on the rotenone exposed PC12 cells and in a neurodegenerative mice model of Parkinson's disease (PD) induced by rotenone. Results show that rotenone caused dose-dependent inhibition of PC12 cell growth with about 50% cell death at 2 µM rotenone. Rotenone caused apoptosis in PC12 cells which was reduced to a notable level by NLC-AS through suppression of oxidative stress, especially via elevation of GSH and total antioxidant capacity, and inhibition of monoamine oxidase. Rotenone significantly augmented neurodegeneration in mouse brains by triggering apoptosis and oxidative damage, while NLC-AS treatment halted these processes. Rotenone-exposed mice showed neuronal deficits and impaired neurocognitive functions like loss of memory and learning restrictions which were restored to a remarkable level by NLC-AS administration. The protective effect of NLC-AS was mediated through the inhibition of GSK3ß and induction of Nrf2 genes in the brain tissues. These findings suggest that NLC-AS administration may efficiently regulate the signs of PD in mice and prevent neurodegeneration and neurocognitive dysfunctions.

Astilbin protects from sepsis-induced cardiac injury through the NRF2/HO-1 and TLR4/NF-κB pathway.

Cardiac dysfunction and arrhythmia are severe complications of sepsis-induced cardiomyopathy and are associated with an increased risk of morbidity and mortality. Currently, the precise mechanism for sepsis-induced myocardial damage remains unclear. Astilbin, a flavonoid, is reported to have anti-inflammatory, antioxidative, and antiapoptotic properties. However, the effects of astilbin on sepsis-induced cardiomyopathy have not been studied so far. This study aims to investigate the effect of astilbin in sepsis-induced myocardial injury and elucidate the underlying mechanism. In vivo and in vitro sepsis models were created using lipopolysaccharide (LPS) as an inducer in H9C2 cardiomyocytes and C57BL/6 mice, respectively. Our results demonstrated that astilbin reduced myocardial injury and improved cardiac function. Moreover, astilbin prolonged the QT and corrected QT intervals, attenuated myocardial electrical remodeling, and promoted gap junction protein (Cx43) and ion channels expression, thereby reducing the susceptibility of ventricular fibrillation. In addition, astilbin alleviated LPS-induced inflammation, oxidative stress, and apoptosis. Astilbin suppressed the toll-like receptor 4 (TLR4)/nuclear factor-κB (NF-κB) pathway in vivo and in vitro models. Astilbin remarkedly upregulated the nuclear factor erythroid 2-related factor 2 (NRF2) and heme oxygenase 1 (HO-1) expression. The in vitro treatment with an NRF2 inhibitor reversed the inhibition of the TLR4/NF-κB pathway and antioxidant properties of astilbin. Astilbin attenuated LPS-induced myocardial injury, cardiac dysfunction, susceptibility to VF, inflammation, oxidative stress, and apoptosis by activating the NRF2/HO-1 pathway and inhibiting TLR4/ NF-κB pathway. These results suggest that astilbin could be an effective and promising therapeutics target for the treatment of sepsis-induced cardiomyopathy.

Natural deep eutectic ready to use extract of astilbin: Super high in vitro bioaccessibility, α-amylase and α-glucosidase enzyme inhibition kinetics.

Astilbin, a natural flavonoid, possesses multiple functionalities, while the poor bioavailability seriously restricts its application in functional food and medicine. Therefore, in this study, a natural deep eutectic solvent (NaDES) with choline chloride: lactic acid (CHCL-LAC) is selected to deliver astilbin by evaluating the bioaccessibility and antioxidant capacity during in vitro gastrointestinal digestion, and the inhibitory effect with underlying mechanism of astilbin-CHCL-LAC against α-amylase/α-glucosidase were investigated. The CHCL-LAC showed significant high astilbin bioaccessibility (84.1% bioaccessible) and DPPH and ORAC antioxidant capacity with 75.7% and 57.7% respectively after 3 h in vitro digestion, which may be attributed by hydrogen bond based supramolecule formed between astilbin and CHCL-LAC. Moreover, significant inhibitions of astilbin-CHCL-LAC on α-amylase (IC50 of 0.67 g/L) and α-glucosidase (IC50 of 0.64 g/L) were observed in mixed competitive and non-competitive manners. The dominant binding force between enzymes and astilbin were the hydrogen and hydrophobic interaction. This is the first time that the underlying mechanisms for astilbin delivered by NaDESs were revealed, suggesting that CHCL-LAC-based NaDESs are promising ready-to-use vehicles of natural inhibitors for carbohydrate-hydrolyzing enzymes.

Astilbin targeted Sirt1 to inhibit acetylation of Nrf2 to alleviate grass carp hepatocyte apoptosis caused by PCB126-induced mitochondrial kinetic and metabolism dysfunctions.

3, 3', 4, 4', 5-pentachlorobiphenyl (PCB126) is extensively utilized in electronic products, lubricant, and insecticide due to its excellent chemical stability and insulation prosperity, resulting in its frequent detection in environment. In addition, atmospheric deposition, as well as industrial and urban wastewater discharge can also lead to PCB126 contamination in marine environment, triggering damages to the tissues of aquatic organisms through oxidative stress. Astilbin is a type of flavonoid compound found in plants that plays a crucial role in providing powerful antioxidant and anti-inflammatory properties. In this study, we aimed to investigate the specific mechanism of PCB126-induced damage and the potential protective effect of Astilbin. To achieve this, we treated grass carp hepatocytes (L8824) with 75 µM PCB126 and/or 0.5 mM Astilbin for 24 h and used experimental methods such as Flow cytometry, molecular docking, PPI analysis, detection of commercial kits (ATP concentration and ATPnase activity) and measurement of mitochondrial membrane potential (ΔΨm). Our findings revealed that PCB126 exposure resulted in a decrease in expression levels of Sirt1, factors related to mitochondrial fusion (Opa1, Mfn1, and Mfn2), antioxidant (CAT, SOD1, and SOD2), energy metabolism (PKM2, IDH, and SDH) and anti-apoptosis (Bcl-2), and an increase in expression levels of Nrf2 acetylation, mitochondrial fission (Drp1), factors that promote apoptosis (Cytc, Bax, Cas9, and Cas3) in L8824 cells. Furthermore, our findings revealed a decrease in ΔΨm, ATP concentration and ATPnase activity and apoptosis levels in L8824 cells. Noteworthy, treatment with Astilbin reversed these results. Molecular docking provides solid evidence for the interaction between Astilbin and Sirt1. In summary, our findings suggested that Astilbin promoted the deacetylation of Nrf2 by interacting with Sirt1, thereby alleviating PCB126-induced mitochondrial apoptosis mediated by mitochondrial dynamics imbalance and energy metabolism disorder through the inhibition of oxidative stress in L8824 cells. Our research has initially revealed the correlation between acetylation and apoptosis induced by PCB126, which provided a foundation for a better comprehension of PCB126 toxicity. Additionally, it expanded the potential application value of Astilbin.

Radioprotective efficacy of Astilbin in mitigating radiation-induced lung injury through inhibition of p53 acetylation.

Radiation-induced lung injury (RILI) is a common side effect in thoracic tumor patients undergoing radiotherapy. At present, there is no ideal radio-protective agent which is widely used in RILI treatment. Astilbin (AST), a bioactive flavonoid, exhibits various biological effects, including anti-inflammatory, antioxidant, and anti-fibrotic activities, which partly result from reducing oxidative stress and inflammation in various pathogenic conditions. However, the protective efficacy of AST to ameliorate RILI has not been reported. In this study, we employed network pharmacology, RNA sequencing, and experimental evaluation to reveal the effects and pharmacological mechanism of AST to treat RILI in vivo and in vitro. We observed that AST reduced radiation-induced apoptosis, DNA damage, inflammatory reactions, and the reactive oxygen species (ROS) level in human normal lung epithelial cells BEAS-2B. Further study showed that AST treatment significantly ameliorated RILI by reducing the radiation-induced pathology changes and inflammatory reaction of lung tissue in C57BL/6J mice. Mechanistically, the expression of epithelial-mesenchymal transition (EMT) markers and radiation-triggered acetylation of the p53 protein were alleviated by AST treatment. Furthermore, AST alleviated the acetylation of p53 after intervention of Trichostatin A (TSA). Our data indicate that AST can alleviate RILI by inhibiting inflammatory reactions and the EMT process through decreasing the expression of p53 acetylation. In conclusion, our study suggests that AST has great potential to be a new protective and therapeutic compound for RILI.

Toxicological profile of the Hymenaea courbaril stem bark hydroalcoholic extract using in vitro bioassays and an alternative in vivo Caenorhabditis elegans model.

Hymenaea genus has been used in folk medicine in Brazil, but few studies investigated its toxicity profile. Thus, the aim of this study was to determine toxicological parameters of Hymenaea courbaril stem bark hydroalcoholic extract by utilizing three cell lines including murine macrophages (RAW 264.7), mouse fibroblast cells (L929) and human lung fibroblast (MRC-5), as well as Salmonella/microsome assay, and in vivo Caenorhabditis elegans model. The predominant detected phytoconstituents in the extract were coumarins, flavonoids, phenolics, tannins and saponins and by HPLC analysis, astilbin (AST) was found to be the main component. The DPPH assay demonstrated that H. courbaril hydroalcoholic extract exhibited potent antioxidant activity, with an IC50 of 3.12 µg/ml. The extract at concentrations of 400 and 800 µg/ml decreased cell viability 48 hr after treatment in L929 and MRC-5 cell lines. In the Raw 264.7 strain, just the highest concentration (800 µg/ml) lowered cell viability within 48 hr following exposure. The concentration of 100 µg/ml did not markedly affect cell viability in the trypan blue assay. In the alkaline comet assay the extract was found to be non-genotoxic. In the Ames test, the extract exhibited low mutagenic potential without metabolic activation, since only the highest concentrations produced an effect. H. courbaril extract only affected the survival of C. elegans at concentrations of 800 and 1600 µl/ml. These findings demonstrate that H. courbaril extract appears to exert low toxicity as evidenced in vitro and mutagenicity assays; however, the biological relevance of the response of C. elegans survival to safety assessments needs further studies.

Integrated network pharmacology and gut microbiome analysis to reveal the mechanism of Qu-Zhuo-Tong-Bi decoction against hyperuricemia and gout.

ETHNOPHARMACOLOGICAL RELEVANCE: Qu-zhuo-tong-bi decoction (QZTBD) is a classic Chinese herbal medicine that has shown therapeutic efficacy in clinical practice against hyperuricemia and gout. However, the potential mechanisms of QZTBD remain poorly investigated. AIM OF THE STUDY: To assess the therapeutic effects of QZTBD on hyperuricemia and gout and to reveal its mechanisms of action. MATERIALS AND METHODS: A Uox-KO mouse model of hyperuricemia and gout was established, and QZTBD was administered at a dosage of 18.0 g/kg/d. Throughout the experimental period, the effects of QZTBD on gout symptoms were monitored and analyzed. The integrated network pharmacology and gut microbiota analysis strategy was conducted to explore the mechanism of QZTBD in the treatment of hyperuricemia and gout. Targeted metabolomic analysis was performed to investigate the variation of amino acids and Spearman's rank correlation analysis was conducted to reveal the relationship between the discrepant bacterial genera and the altered amino acid. Flow cytometry was utilized to analysis the proportion of Th17 and Treg cells, and the production of pro-inflammatory cytokines was measured by ELISA. qRT-PCR and Western blot assay were applied to detect the expression of mRNA and protein respectively. Autodock vina 1.1.2 was used to evaluate the docking interactions. RESULTS: QZTBD treatment showed remarkable efficacy against hyperuricemia and gout with respect to attenuation of disease activity metrics through gut microbiome recovery and intestinal immune homeostasis. The administration of QZTBD significantly elevated the abundance of Allobaculum and Candidatus sacchairmonas, corrected the aberrant amino acid patterns, repaired the impaired intestinal barrier, restored the balance of Th17/Treg cells via PI3K-AKT-mTOR pathway, and reduced the levels of inflammatory cytokines such as IL-1ß, IL-6, TNF-α and IL-17. Fecal microbiota transplantation from QZTBD treated mice demonstrated convincing evidence of efficacy and mechanism of QZTBD. CONCLUSION: Taken together, our study explores the therapeutic mechanism of an effective herbal formula, QZTBD, for gout treatment through remodeling gut microbiome and regulating the differentiation of CD4+ T cells via PI3K-AKT-mTOR pathway.

Attenuative effect of astilbin on polystyrene microplastics induced testicular damage: Biochemical, spermatological and histopathological-based evidences.

Polystyrene microplastics (PS-MPs) are the potential environmental pollutants that possess the ability to induce testicular damage. Astilbin (ASB) is a dihydroflavonol, abundantly reported in multiple plants that has various pharmacological properties. This research elucidated the mitigative potential of ASB against PS-MPs-instigated testicular toxicity. 48 adult male rats (200 ± 10 g) were distributed into 4 groups (n = 12): control, PS-MPs received (0.01 mg/kg), PS-MPs + ASB received (0.01 mg/kg + 20 mg/kg) and ASB supplemented group (20 mg/kg). After 56th day of the trial, animals were sacrificed and testes were harvested for the estimation of biochemical, hormonal, spermatogenic, steroidogenic, apoptotic and histological profiles. PS-MPs intoxication significantly (P < 0.05) lowered glutathione peroxidase (GPx), superoxide dismutase (SOD), glutathione reductase (GSR) as well as catalase (CAT) activities, whereas elevated MDA as well as ROS levels. Besides, the levels of interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), interleukin-1ß (IL-1ß), nuclear factor kappa-B (NF-κB) along with cyclooxygenase-2 (COX-2) activity were raised. PS-MPs treatment reduced luteinizing hormone (LH), plasma testosterone and follicle-stimulating hormone (FSH) level besides decreased epididymal sperm number, viability, motility as well as the count of HOS coil-tailed spermatozoa and increased sperm morphological irregularities. PS-MPs exposure lowered steroidogenic enzymes (17ß-HSD, 3ß-HSD and StAR protein along with Bcl-2 expression, besides increasing Caspase-3 and Bax expressions and histopathological alterations in testicular tissues. However, ASB treatment significantly reversed PS-MPs mediated damage. In conclusion, ASB administration is protective against PS-MPs-instigated testicular damage owing to its anti-inflammatory, anti-apoptotic, antioxidant and androgenic nature.

Antioxidant and In Vivo Hypoglycemic Activities of Ethanol Extract from the Leaves of Engelhardia roxburghiana Wall, a Comparative Study of the Extract and Astilbin.

The leaves of Engelhardia roxburghiana Wall (LERW) has been used as sweet tea in China throughout history. In this study, the ethanol extract of LERW (E-LERW) was prepared and the compositions were identified by HPLC-MS/MS. It indicates that astilbin was the predominant component in E-LERW. In addition, E-LERW was abundant in polyphenols. Compared to astilbin, E-LERW presented much more powerful antioxidant activity. The E-LERW also had stronger affinity with α-glucosidase and exerted more vigorous inhibitory effect on the enzyme. Alloxan-induced diabetic mice had significantly elevated glucose and lipid levels. Treatment with E-LERW at the medium dose (M) of 300 mg/kg could reduce the levels of glucose, TG, TC, and LDL by 16.64%, 12.87%, 32.70%, and 22.99%, respectively. In addition, E-LERW (M) decreased food intake, water intake, and excretion by 27.29%, 36.15%, and 30.93%, respectively. Moreover, E-LERW (M) therapy increased the mouse weight and insulin secretion by 25.30% and 494.52%. With respect to the astilbin control, E-LERW was more efficient in reducing the food and drink consumption and protecting pancreatic islet and body organs from alloxan-induced damage. The study demonstrates that E-LERW may be a promising functional ingredient for the adjuvant therapy of diabetes.

Citric Acid Enhances the Activities of Astilbin on Psoriasis via Down-Regulation of P-Glycoprotein.

Astilbin (AS) has been confirmed to be an attractive candidate drug for psoriasis; however, the low oral absorption limits its further development and utilization. Herein, a simple method was discovered to solve this problem, which was combined with citric acid (CA). The efficiency was estimated by imiquimod (IMQ)-induced psoriasis-like mice, and the absorption was predicted by the Ussing chamber model, HEK293-P-gp cells were used to validate the target. Compared with the AS group, the combination with CA significantly reduced the PASI score and down-regulated the protein expression of IL-6 and IL-22, which showed that the combination of CA enhanced the anti-psoriasis effect of AS. Moreover, AS concentration in psoriasis-like mice plasma was significantly increased (3.90-fold) in the CA combined group, and the mRNA and protein levels of P-gp in the small intestine of the combined group were decreased by 77.95 and 30.00%, respectively. In addition, when combined with CA, AS absorption significantly increased while the efflux ratio decreased in vitro. Furthermore, CA significantly elevated the uptake of AS by 153.37% and decreased the protein expression of P-gp by 31.70% in HEK293-P-gp cells. These results indicated that CA enhanced the therapeutic efficacy of AS by improving its absorption via down-regulation of P-gp.

Alpha-glucosidase inhibitory activities of astilbin contained in Bauhinia strychnifolia Craib. stems: an investigation by in silico and in vitro studies.

INTRODUCTION: Bioactive compounds from traditional medicines are good alternatives to standard diabetes therapies and may lead to new therapeutic discoveries. The stems of Bauhinia strychnifolia Craib. (BC) have a possible antihyperglycemic effect; However, the extraction of astilbin from BC has never been recorded in alpha-glucosidase inhibitory activities. METHODS: Using liquid chromatography-mass spectrometry (LC-MS/MS), 32 compounds were detected in the BC extract. The screening was based on peak area. Seven compounds found. PASS recognized all seven compounds as potential alpha-glucosidase (AG) inhibitors. Astilbin and quercetin 3-rhamnoside were the most likely inhibitors of AG. Arguslab, AutoDock, and AutoDock Vina investigated the binding of the two compounds and AG. The binding stability was confirmed by molecular dynamics (MD). In addition, the optimum solvent extraction was studied via CosmoQuick, and extracts were examined with 1H-NMR prior to testing with AG. RESULTS: All three software programs demonstrated that both compounds inhibit AG more effectively than acarbose. According to the sigma profile, THF is recommended for astilbin extraction. The BC extract with THF showed outstanding AG inhibitory action with an IC50 of 158 ± 1.30 µg mL-1, which was much lower than that of the positive control acarbose (IC50 = 190 ± 6.97 µg mL-1). In addition, astilbin from BC was found to inhibit AG strongly, IC50 = 22.51 ± 0.70 µg mL-1 through the extraction method of large-scale astilbin with THF has the best extraction capacity compared to other solvents, hence the initial stage of extraction employs THF to extract and precipitate them with ethyl acetate and water. CONCLUSION: In silico and in vitro studies reveal that astilbin inhibits AG and is superior to acarbose, validating its promise as an AG inhibitor. Overall, astilbin was the most bioactive component of BC for antidiabetic action.

First report of phenolic compounds isolated from Inga stipularis DC. (fabaceae) leaves.

Several species of the Inga genus are used by Amazonian indigenous communities to treat injuries, pain and inflammations, which is directly related to the presence of phenolic compounds in these species. Many studies have addressed the phytochemical relevance of this genus, but they are still few considering the large number of species. Therefore, this study aimed to investigate the chemical composition of Inga stipularis leaves in order to find compounds with potential pharmacological application and economic interest. The developed method allowed the isolation and identification of 8 compounds in the ethanol extract of I. stipularis: eucryphin, neoastilbin, astilbin, neoisoastilbin, isoastilbin, quercitrin, engeletin and isoengeletin. Astilbin stands out for having been isolated directly from the fractionation of the extract by SPE with high yield. This study was a pioneer for I. stipularis and revealed the potential of the species as an abundant source of compounds of pharmacological and economic interest.

Astilbin Attenuates Cadmium-Induced Adipose Tissue Damage by Inhibiting NF-κB Pathways and Regulating the Expression of HSPs in Chicken.

Cadmium (Cd) can damage tissues by inducing oxidative stress, lymphocyte infiltration, and inflammation in these sites. Meanwhile, astilbin (Ast) is an antioxidant agent. At present, only a few mechanisms of Cd-induced adipose tissue damage have been described. Herein, we assessed the potential protective effects and the molecular mechanism underlying the antioxidant properly of Ast after Cd intake in chicken adipose tissue. In this study, a total of 160 7-day-old roosters were randomly divided into four groups. Roosters were fed with a basic diet (C group), Ast 40 mg/kg (Ast group), CdCl2 150 mg/kg + Ast 40 mg/kg (Cd/Ast group), and CdCl2 150 mg/kg (Cd group) for 60 days. We found that Cd intake changed the morphology and structure of adipose tissues and decreased the expression of several antioxidants, including total superoxide dismutase (T-SOD), glutathione peroxidase (GSH-Px), catalase (CAT), and total antioxidant capacity (T-AOC), but increased those of oxidative stress markers including malondialdehyde (MDA), inducible nitric oxide synthase (iNOS), NO, and H2O2. Cd further activated the nuclear factor kappa B (NF-κB) signaling pathway and increased the expression of the inflammation-related mediators, interleukin 1beta (IL-1ß), interleukin 6 (IL-6), interleukin 8 (IL-8), interleukin 10 (IL-10), cyclooxygenase-2 (COX-2), iNOS, prostaglandin E synthase (PTGES), tumor necrosis factor-alpha (TNF-α), and interferon-gamma (IFN-γ). Cd-induced oxidative stress upregulated the expression of three heat shock proteins (HSPs), including HSP27, HSP70, and HSP90. Summarily, Cd causes oxidative stress-mediated tissue damage by activating the NF-κB pathway, promoting inflammation and upregulating the expression of HSPs. However, Ast supplementation modulates oxidative stress in adipose tissue by inhibiting inflammation mediated by the NF-κB pathway and regulating the expression of HSPs.

The natural source, physicochemical properties, biological activities and metabolism of astilbin.

Astilbin is a dihydroflavanol found in many plants and processed foods. Astilbin possesses multiple health-beneficial bioactivities and has received great attention. Hence, the natural source, physicochemical properties, biological activities and metabolism of astilbin are summarized in the present article. Engelhardia roxburghiana Wall. and Smilax glabra Roxb. are the main resource for astilbin purification because of high content. Because of chemical instability, astilbin amount in foods is dependent on the processing and storage conditions. The degradation of astilbin includes isomerization and decomposition. The interconversion of astilbin and its isomers occurs through a chalcone intermediates, which significantly affects the taste of wine during storage. Many factors such as temperature, pH, metal ions and food additives could affect the chemical stability of astilbin. Astilbin exhibits very novel selective immunosuppressive activity, which is not found in other compounds. The rhamnose moiety of astilbin is essential for this bioactivity. After digestion, astilbin was mainly absorbed and transported in circulatory blood in its intact form, and only one metabolite, 3'-O-methylastilbin, was found. Although having many bioactivities, astilbin faces the challenge of poor bioavailability. Some promising strategies were developed for improving its bioavailability, particularly through fabrication the zein nanoparticles.