The nutritional profile of chia seeds and sprouts: tailoring germination practices for enhancing health benefits-a comprehensive review.

Chia seeds have gained significant attention due to their unique composition and potential health benefits, including high dietary fibers, omega-3 fatty acids, proteins, and phenolic compounds. These components contribute to their antioxidant, anti-inflammatory effects, as well as their ability to improve glucose metabolism and dyslipidemia. Germination is recognized as a promising strategy to enhance the nutritional value and bioavailability of chia seeds. Chia seed sprouts have been found to exhibit increased essential amino acid content, elevated levels of dietary fiber and total phenols, and enhanced antioxidant capability. However, there is limited information available concerning the dynamic changes of bioactive compounds during the germination process and the key factors influencing these alterations in biosynthetic pathways. Additionally, the influence of various processing conditions, such as temperature, light exposure, and duration, on the nutritional value of chia seed sprouts requires further investigation. This review aims to provide a comprehensive analysis of the nutritional profile of chia seeds and the dynamic changes that occur during germination. Furthermore, the potential for tailored germination practices to produce chia sprouts with personalized nutrition, targeting specific health needs, is also discussed.

Gli1-mediated tumor cell-derived bFGF promotes tumor angiogenesis and pericyte coverage in non-small cell lung cancer.

BACKGROUND: Tumor angiogenesis inhibitors have been applied for non-small cell lung cancer (NSCLC) therapy. However, the drug resistance hinders their further development. Intercellular crosstalk between lung cancer cells and vascular cells was crucial for anti-angiogenenic resistance (AAD). However, the understanding of this crosstalk is still rudimentary. Our previous study showed that Glioma-associated oncogene 1 (Gli1) is a driver of NSCLC metastasis, but its role in lung cancer cell-vascular cell crosstalk remains unclear. METHODS: Conditioned medium (CM) from Gli1-overexpressing or Gli1-knockdown NSCLC cells was used to educate endothelia cells and pericytes, and the effects of these media on angiogenesis and the maturation of new blood vessels were evaluated via wound healing assays, Transwell migration and invasion assays, tube formation assays and 3D coculture assays. The xenograft model was conducted to establish the effect of Gli1 on tumor angiogenesis and growth. Angiogenic antibody microarray analysis, ELISA, luciferase reporte, chromatin immunoprecipitation (ChIP), bFGF protein stability and ubiquitination assay were performed to explore how Gli1 regulate bFGF expression. RESULTS: Gli1 overexpression in NSCLC cells enhanced the endothelial cell and pericyte motility required for angiogenesis required for angiogenesis. However, Gli1 knockout in NSCLC cells had opposite effect on this process. bFGF was critical for the enhancement effect on tumor angiogenesis. bFGF treatment reversed the Gli1 knockdown-mediated inhibition of angiogenesis. Mechanistically, Gli1 increased the bFGF protein level by promoting bFGF transcriptional activity and protein stability. Importantly, suppressing Gli1 with GANT-61 obviously inhibited angiogenesis. CONCLUSION: The Gli1-bFGF axis is crucial for the crosstalk between lung cancer cells and vascular cells. Targeting Gli1 is a potential therapeutic approach for NSCLC angiogenesis.

Overview of distinct 5-methylcytosine profiles of messenger RNA in normal and knock-down NSUN2 colorectal cancer cells.

Background: Colorectal cancer (CRC) is a harmful cancer with high morbidity and poor prognosis. There is growing evidence that RNA methylation is closely related to the occurrence of cancer and its malignant biological behavior. N6-methyladenosine (m6A) methylation is the most common RNA modification in eukaryotes, and its multiple regulatory mechanisms in CRC have been elucidated from multiple perspectives. At the same time, the role of 5-methylcytosine (m5C), another important and widely distributed methylation modification, in CRC is far from being elucidated. Methods: In this study, we used RNA immunoprecipitation sequencing combined with bioinformatics methods to identify the m5C peaks on messenger RNA (mRNA) in HCT15 cells and sh-NSUN2 HCT15 cells, understand which transcripts are modified by m5C, and characterize the distribution of m5C modifications. In addition, we performed further bioinformatics analysis of the detected data to initially clarify the potential function of these m5C-modified transcripts. Results: We found significant differences in the distribution of m5C between HCT15 cells and sh-NSUN2 HCT15 cells, suggesting that m5C is likely to play a key role in the occurrence and development of CRC. Furthermore, Gene Ontology (GO) enrichment analysis showed that genes altered by m5C were mainly enriched in phylogeny, synaptic membrane, and transcription factor binding. The Kyoto Encyclopedia of Genes and Genomes (KEGG)pathway analysis showed that the genes altered by m5C are enriched in ECM receptor interaction pathway, the circadian pathway, and the cAMP signaling pathway. Conclusion: Here, our study preliminarily revealed the different distribution patterns of m5C between HCT15 cell and sh-NSUN2 HCT15 cell. Our results open a new window to understand the role of m5C RNA methylation of mRNA in the development of CRC.

Naringenin Inhibits Platelet Activation and Arterial Thrombosis Through Inhibition of Phosphoinositide 3-Kinase and Cyclic Nucleotide Signaling.

Citrus flavanoids intake can reduce the risk of cardiovascular diseases. Naringenin, a natural predominant flavonoid abundant in citrus fruits, possesses protective effects against atherothrombotic diseases. As platelet activation plays central roles in atherothrombogenesis, we studied the effects of naringenin on platelet activation, signaling, thrombosis and hemostasis. Naringenin dose-dependently inhibited agonist-induced platelet aggregation in vitro, and exhibited more-potent efficacy on ADP-induced platelet aggregation. It also suppressed platelet aggregation stimulated by ADP ex vivo. Naringenin inhibited ADP-induced platelet α-granule secretion, fibrinogen binding, intracellular calcium mobilization and platelet adhesion on collagen-coated surface. Naringenin also inhibited platelet spreading on fibrinogen and clot retraction, processes mediated by outside-in integrin signaling. Mechanism studies indicated that naringenin suppressed PI3K-mediated signaling and phosphodiesterase activity in platelets, in addition to increasing cGMP levels and VASP phosphorylation at Ser239. Furthermore, naringenin-induced VASP phosphorylation and inhibition of platelet aggregation were reversed by a PKA inhibitor treatment. Interestingly, naringenin inhibited thrombus formation in the (FeCl3)-induced rat carotid arterial thrombus model, but not cause a prolonged bleeding time in mice. This study suggests that naringenin may represent a potential antiplatelet agent targeting PI3K and cyclic nucleotide signaling, with a low bleeding risk.

Prevention of platelet aggregation and arterial thrombosis using a modified Shenzhu Guanxin Formula.

OBJECTIVE: Modified Shenzhu Guanxin Formula (mSGF) has beneficial effects in coronary artery disease. Previously, we found that mSGF inhibited platelet aggregation in rats. In the present study we further investigated the antiplatelet and antithrombotic activities of mSGF in rats. METHODS: Rats were orally administered mSGF (4.2, 8.4, or 16.8 g crude drug/kg), the adenosine 5'-diphosphate (ADP) receptor antagonist clopidogrel (7.875 mg/kg), or saline once a day for 7 days. The effects of mSGF on platelet aggregation were measured. Levels of cyclic adenosine monophosphate (cAMP) and phosphoinositide 3-kinase (PI3K) signaling were analyzed by ELISA and western blotting, respectively. The antithrombotic effect of mSGF was investigated using a FeCl3-induced carotid arterial thrombosis model and effects on bleeding time were assessed in a rat tail transection model. RESULTS: mSGF significantly inhibited ADP-induced platelet aggregation in a dose-dependent manner, elevated cAMP levels and inhibited phosphorylation of extracellular signal-regulated kinase (ERK) and PI3K/protein kinase B (Akt). Moreover, mSGF dose-dependently inhibited thrombosis in a FeCl3-induced carotid arterial thrombus model and had a significantly smaller effect on bleeding time compared with clopidogrel. CONCLUSIONS: mSGF represents a potent and safe antithrombotic agent whose antiplatelet activity is probably mediated through blockade of PI3K/Akt signaling and increased cAMP generation.

Investigating the interaction between three perfluorinated carboxylic acids and the G protein-coupled estrogen receptor: spectroscopic analyses and computational simulations.

In this paper, perfluorinated compounds (PFCs), such as perfluorobutyric acid (PFBA), perfluorooctanoic acid (PFOA) and perfluorododecanoic acid (PFDoA), were selected as typical representatives of perfluorinated carboxylic acids (PFCAs) to study the effects of PFCAs on the G protein-coupled estrogen receptor (GPER). The interaction mechanism of the three types of PFCAs with the GPER was investigated using steady-state fluorescence spectroscopy, ultraviolet-visible spectroscopy, three-dimensional fluorescence spectroscopy, and Fourier transform infrared spectroscopy combined with molecular docking and molecular dynamics simulations. Among these techniques, steady-state fluorescence and ultraviolet-visible spectroscopic analyses showed that PFBA, PFOA and PFDoA quenched the endogenous GPER fluorescence by combined dynamic and static quenching and non-radiative energy transfer. The binding constants (Ka) of PFCAs on the GPER were all larger than 105 L mol-1, indicating that their affinity for the GPER was strong. Fourier transform infrared spectroscopy and three-dimensional fluorescence showed that the secondary structure of the GPER changed after binding to PFCAs. Thermodynamic analysis showed ΔG < 0, which indicated that the interaction between the GPER and PFCAs was spontaneous. For the binding of PFBA and PFOA to the GPER, ΔH > 0 and ΔS > 0, indicating that the interaction was mainly driven by hydrophobic forces; for the binding of PFDoA to the GPER, ΔH < 0 and ΔS < 0, suggesting that van der Waals force and hydrogen bonding were the main interaction forces. Molecular dynamics simulations suggested that the stability of the GPER-PFCA complexes was higher than that of the free GPER, and also that the structure and hydrophobicity of the GPER changed after binding to PFCAs. Molecular docking analysis showed that all three PFCAs could form hydrogen bonds with the GPER, which improved the stability of the complex.

Dynamic Changes of Beclin-1 in the Hippocampus of Male Mice with Vascular Dementia at Different Time Points.

This study tried to investigate the dynamic changes of Beclin-1 in the hippocampus of male mice with vascular dementia (VD) at different time points. The mouse model of VD was established by the four-vessel blocking method. Then, the VD mice were randomly divided into five groups (n = 12) according to the disease duration: the 0.1-day model group, 0.5-day model group, 1-day model group, 3-day model group, 5-day model group and 14-day model group. In addition, all surgical procedures were the same in the sham group as those in the model groups, except the mice in the sham group were not subjected to clipping. The expression of Beclin-1, LC3B, p62, Bcl-2, Bax, BACE1, GFAP, MBP and ET-1 mRNA were determined by RT-PCR; the expression of Beclin-1 was detected by Western blot and immunofluorescence; the pathological characteristics of the hippocampus were observed by haematoxylin-eosin (HE) staining; and the correlation of Beclin-1 with other VD-related proteins was analysed by Pearson's correlation. Compared with that in the sham group, the expression of Beclin-1, LC3B, Bax, BACE1, GFAP, MBP and ET-1 mRNA was increased in the VD mice at different time points (0.1 day, 0.5 day, 1 day, 3 days, 5 days and 14 days) (P < 0.05) and then remained relatively stable in the 0.5-day VD mice, whereas the p62 and Bcl-2 mRNA levels decreased (P < 0.05). Beclin-1 protein expression was significantly increased in the VD mice at different time points (P < 0.05). The hippocampus showed a certain degree of neuronal damage in the VD mice at different time points (P < 0.05). Additionally, certain correlations among LC3B, p62, Bcl-2, Bax, BACE1, GFAP, MBP, ET-1 and Beclin-1 were observed in this study. In conclusion, the results described above demonstrated that neuronal damage and dynamic stability of Beclin-1 expression were established in the VD male mice after 0.5 day by the four-vessel blocking method.

Ginsenoside Rb1 prevents homocysteine-induced EPC dysfunction via VEGF/p38MAPK and SDF-1/CXCR4 activation.

Hyperhomocystinemia (HHcy) is known as an independent risk factor for cardiovascular disease. Our previous study showed that ginsenoside Rb1, the major active constituent of ginseng, prevents homocysteine (Hcy)-induced endothelial damage. However, the role of ginsenoside Rb1 in Hcy-induced dysfunction in endothelial progenitor cells (EPCs) remains unknown. In the study, we found that ginsenoside Rb1 reversed the Hcy-induced impairment of adhesive and migratory ability in EPCs which were significantly abolished by CXCR4 antagonist AMD3100 and VEGFR2 inhibitor SU5416. Ginsenoside Rb1 significantly reversed Hcy-induced SDF-1 reduction in the supernatant and in the serum. Ginsenoside Rb1 reversed downregulation of SDF-1 and VEGFR2 protein expression, inhibition of p38MAPK phosphorylation induced by Hcy. Re-endothelialization in balloon-injured carotid arteries significantly increased with EPCs transplant, and was even better with Rb1 treatment. This effect was significantly abolished by AMD3100. AMD3100 also decreased the number of CM-DiI labeled EPCs in injured arteries. Here we show for the first time that Rb1 prevents Hcy-induced EPC dysfunction via VEGF/p38MAPK and SDF-1/CXCR4 activation. These findings demonstrate a novel mechanism of the action of Rb1 that may have value in prevention of HHcy associated cardiovascular disease.

[Application of molecular biotechnology in Pharmacognosy].

Using the methods of informetrics analysis, articles retrieved from the database of CNKI were statistically analyzed on development course and knowledge system, so as to reflect the overall situation of pharmacognostical studies by molecular biotechnology. The result shows that the research on pharmacognosy by molecular biotechnology is an inter-disciplinary research area, the major research fields can be divided into 7 categories, including molecular identification of Chinese medicinal materials, molecular systematics and genetic diversity analysis of Chinese medicinal materials, biosynthesis and bioregulation of secondary metabolites in medicinal plants, molecular mechanism and genetic basis of Dao-di Herbs, and tissue culture and molecular breeding in medicinal plants. The research on pharmacognosy by molecular have achieved remarkable progress in recent 20 years, and have broad development prospects.

[Development of molecular pharmacognosy in China based on bibliometric analysis].

The method of bibliometrics was used to analyze the literature about the application of molecular biotechnique to pharmacognosy which were searched and obtained from the CNKI database and Shanghai intellectual property information platform from the year 1995 to 2015.It was found that 22 462 articles were published and the 63% were funded, 50 core institutions and 888 authors, 18 core journals were engaged in this subject.496 items of patents were authorized and 90 kinds of Chinese Materia Medica were involved.In the view of the quantity and quality of published literature, the scale and influence of journals, institutions, and the extent of subject categories have made remarkable achievement. Molecular pharmacognosy has completed the germination stage of a new subject, and has been in a relatively mature and stable development status.

[Metabonomics Study on Urine 1H-NMR in Chronic Superficial Gastritis Patients with Pi-qi Deficiency Syndrome/Pi-Wei Dampness-heat Syndrome].

OBJECTIVE: To observe metabolomic changes in urine of chronic superficial gastritis (CSG) patients with Pi-qi deficiency syndrome (PQDS) or Pi-Wei dampness-heat syndrome (PWDHS), thereby providing scientific evidence for syndrome typing of them. METHODS: Urine samples were collected from CSG patients with PQDS/PWDHS and healthy volunteers, 10 in each group. Proton nuclear magnetic resonance spectroscopy (1H-NMR) based metabonomic analysis was performed on urine samples. Contents of related biomarkers were analyzed by principal component analysis (PCA), partial least square discriminant analysis (PLS-DA), and urivariate statistical analysis. RESULTS: PLS-DA analysis showed that metabolites among CSG patients with PQDS/PWDHS and healthy volunteers could be mutually distinguished. Seven differentially identified metabolites were screened from urines of CSG patients with PQDS and healthy volunteers included glutamate, methionine, α-oxoglutarate, dimethylglycine, creatinine, taurine, and glucose. Four differentially identified metabolites were screened from urines of CSG patients with PWDHS and healthy volunteers included 2-hydroxybutyric acid, trimethylamine oxide, taurine, and hippuric acid. Eleven differentially identified metabolites were screened from urines of CSG patients with PQDS and PWDHS included fucose, ß-hydroxybutyric acid, alanine, glutamate, methionine, succinic acid, citric acid, creatinine, glucose, hippuric acid, and lactic acid. CONCLUSION: The metabolic differences of CSG patients PQDS and PWDHS mainly manifested in glycometabolism, lipid metabolism, and amino acids catabolism, and 1H-NMR based metabonomics may be used in classified study of Chinese medical syndrome typing.

Effect of estrogen on gene expression of fatty acid synthase in periosteum.

BACKGROUND: Estrogen deficiency contributes to postmenopausal osteoporosis. Periosteum might be a potential target of estrogen, but the underlying mechanism at gene level is far from being elucidated. The objective of this study was to investigate the correlation between estrogen and fatty acid synthase (FAS) expression in periosteum. METHODS: Human periosteum cells were cultured in vitro. Expressed genes in the substrated cDNA library were verified using semi-quantitative PCR and real-time PCR. The expression of FAS in periosteum of ovarectomized (OVX) SD rats was investigated. RESULTS: FAS gene was most significantly expressed in the subtracted cDNA library of periosteal cells screened by semi-quantitative PCR. Low FAS expression was verified by real-time PCR in the estrogen exposed human periosteum rather than in the control. The estradiol levels were (20.81 +/- 12.62) pg/ml, (19.64 +/- 4.35) pg/ml and (13.47 +/- 1.84) pg/ml in the sham group, the control, and the OVX group, respectively. The estradiol levels in the OVX group was significantly lower (P = 0.0386). The FAS gene expression in periosteum in the OVX group, sham group, and control group was 3.09 +/- 1.97, 1.33 +/- 0.47 and 1.51 +/- 1.32, respectively. The gene expression in the OVX group was significantly higher (P = 0.0372). CONCLUSION: Estrogen modulates FAS gene expression in in vitro human perisoteum as well as in in vivo rat periosteum.

[Monitoring the breast changes of Chinese postmenopausal women under long-term hormone replacement therapy by mammary ultrasonography].

OBJECTIVE: To investigate the effects of long-term hormone replacement therapy (HRT) on the breasts of postmenopausal women using mammary ultrasonography. METHODS: An open randomized clinical study was designed. The percutaneous estradiol gel was used in a cyclic regimen combined with micronized progesterone (MP) or medroxyprogesterone acetate (MPA). Sixty healthy women (natural menopause for 1 to 5 years) were recruited and divided into four groups according to the dosage of estrogen and two kinds of progestin. All were given for 25 days per month. Mammary ultrasonography was used to observe breast glandular section thickness, breast duct width, the morphology of lobular unit and the blood flow of color Doppler imaging at baseline and every year from the second to seventh year of HRT. The serum estradiol was also measured from the 15th to 25th day of the cycle. Breast pain was recorded by the subjects. RESULTS: (1) The breast glandular section thickness after HRT was larger than that of before HRT. The breast glandular section thickness became larger gradually over time while the breast duct width became smaller over time. The breast duct width of the fifth year of HRT was significantly different from that of the sixth year (P < 0.05). (2) Twenty-two persons had new breast structure changes after HRT, and the accumulated incidence was 41.5%. New solid lesions formation occurred in five subjects (8.3%) and new cyst formation occurred in one subject (1.7%). After the second year of HRT, the serum estradiol level of the subjects with breast structure changes was higher than that of without breast structure changes and in the sixth year of HRT, and the difference was significant (P < 0.05). After the second year of HRT, the breast glandular section thickness of the subjects with breast structure changes was larger than that of without breast structure changes and in the fifth and sixth year of HRT, the difference was significant (P < 0.05). (3) After HRT, the serum estradiol level of subjects with mastalgia was higher than that of without mastalgia and in the second and sixth follow-up year, the difference was significant (P < 0.05). CONCLUSIONS: There is an increasing trend of the percentage of glandular tissues of the breast after HRT. There is an increasing trend of the serum estradiol level and the breast glandular section thickness among the subjects with the breast structure changes; there is an increasing trend of the serum estradiol level among the subjects with mastalgia. Mammary ultrasonography can be used to monitor breast structure changes and breast lesions during HRT.