Polyporus umbellatus is a traditional medicinal fungus with potential application as a food-related bioactive; however, toxicological data for concentrated extracts remain limited. This study evaluated aqueous P. umbellatus extract using three complementary genotoxicity assays and a 2-week repeated-dose toxicity study. Genotoxicity was assessed using an in vitro chromosomal aberration assay in Chinese hamster lung cells, a bacterial reverse mutation assay, and an in vivo bone marrow micronucleus assay. The repeated-dose toxicity study was performed in F344 rats administered 500, 1000, or 2000 mg/kg/day P. umbellatus extract by oral gavage for 2 weeks. P. umbellatus extract significantly increased structural chromosomal aberrations in vitro under short-term treatment with metabolic activation, and under short-term and continuous-treatment conditions without metabolic activation. In contrast, the extract did not increase revertant colonies of Salmonella typhimurium or Escherichia coli tester strains, and oral administration did not increase micronucleated polychromatic erythrocytes in male or female ICR mice. Repeated oral administration for 2 weeks caused no mortality, treatment-related clinical signs, body weight loss, gross lesions, or consistent hematological or serum biochemical toxicity patterns. Isolated changes in male kidney weight, female salivary gland weight, and male creatine kinase activity were not accompanied by concordant findings and were therefore not interpreted as definitive adverse effects. Overall, the findings indicate an in vitro clastogenic response without evidence of bacterial mutagenicity, bone marrow micronucleus induction, or overt repeated-dose oral toxicity under the investigated experimental conditions, paving the way for long-term studies to complete the toxicological characterization of P. umbellatus.
Helicobacter pylori remains a major cause of chronic gastritis and dyspeptic symptoms, and the effectiveness of standard eradication therapy continues to decline with increasing antibiotic resistance. Lacticaseibacillus paracasei HP7 has shown inhibitory and anti-inflammatory effects on H. pylori in preclinical studies. This study investigated whether 8-week oral HP7 supplementation could improve H. pylori-related outcomes in adults with confirmed infection. Seventy-eight adults with positive 13C-urea breath test (13C-UBT) results and gastric discomfort were randomized to receive low-dose HP7 (HP7-L, 1.5 × 109 CFU/day), high-dose HP7 (HP7-H, 5.0 × 109 CFU/day), or placebo for 8 weeks. Outcomes included changes in 13C-UBT values, upper gastrointestinal (GI) symptoms assessed by Korean Gastrointestinal Symptom Rating Scale, pepsinogen I/II ratio, serum tumor necrosis factor-α, and quality-of-life indices. HP7-H significantly reduced 13C-UBT values compared with placebo. HP7 supplementation was also associated with improvements in gastric mucosal biomarkers and modest changes in selected upper GI symptom and quality-of-life domains. Overall microbial diversity was not significantly altered, although the abundance of L. paracasei increased following supplementation. No treatment-related serious adverse events were observed, and all laboratory findings remained within clinical reference ranges. Complete eradication of H. pylori was not achieved in most participants. These findings support the clinical potential of HP7 supplementation to attenuate H. pylori-related activity and improve gastric biomarkers, with modest benefits in selected dyspeptic symptom domains. HP7 may be a safe and effective functional food option for H. pylori management when antibiotics are contraindicated or ineffective. Further studies are warranted to confirm long-term efficacy and durability of these effects.
Dyslipidemia is a significant risk factor for cardiovascular disease. This study evaluated the efficacy of a cholesterol-lowering diet, a supplement containing bergamot and plant sterols, and their combination in managing dyslipidemia. In this 12-week randomized controlled trial, 61 adults with dyslipidemia were assigned to one of three groups: diet-only (Group D, n = 19), supplement-only (Group B, n = 21; 150 mg bergamot flavonoids + 800 mg plant sterols/day), or mixed (Group M, n = 21; Diet + Supplement). Efficacy was assessed via changes in biochemical and anthropometric parameters. The primary finding was the superior efficacy of the mixed group (Group M), which demonstrated significantly greater reductions in total cholesterol (-53.9 mg/dL; -19.8%), low-density lipoprotein cholesterol (LDL-C) (-42.6 mg/dL; -23.3%), and triglycerides (TGs) (-57.2 mg/dL; -29.7%) compared to both diet-only and supplement-only groups (P < .05). While all three groups showed improved total and LDL-C, TG levels decreased significantly only in the supplement-receiving groups (Group B and Group M). Conversely, dietary intervention primarily drove significant improvements in body weight (Group D: -4.2 kg; Group M: -3.4 kg), body mass index (-1.5 and -1.2 kg/m2, respectively), and fat mass (-3.5 and -2.9 kg, respectively). High-density lipoprotein cholesterol and liver enzymes (alanine aminotransferase, aspartate aminotransferase) remained unchanged across all groups. Combining a cholesterol-lowering diet with a bergamot and plant sterol supplement offers a synergistic and superior strategy for improving the lipid profile in individuals with dyslipidemia, while the dietary component remains essential for improving body composition.
Baccharis dracunculifolia, the main botanical source of Brazilian green propolis, has gained prominence as a versatile medicinal species due to its rich profile of phenolic acids, flavonoids, and terpenoids with recognized antioxidant and anti-inflammatory properties. This review synthesizes experimental evidence on how different preparations of B. dracunculifolia, including hydroalcoholic, ethanolic, glycolic, methanolic, n-hexane and ethyl acetate extracts, and essential oil, modulate redox balance, inflammatory, and immunomodulatory responses in vitro and in vivo. Emphasis is placed on metabolites such as caffeic and p-coumaric acids, artepillin C, baccharin, isosakuranetin, and nerolidol, which contribute to reactive oxygen species scavenging, preservation of mitochondrial function, reinforcement of endogenous antioxidant defenses, and inhibition of enzymes like myeloperoxidase, nicotinamide adenine dinucleotide phosphate oxidase oxidase, and cyclooxygenase-2. The impact of seasonality, plant part, solvent, and extraction technique on phytochemical composition and mechanisms of biological activity is presented in preclinical models of colitis, gastric ulcer, arthritis, hepatotoxicity, cardiometabolic syndrome, diabetes, and inflammatory skin diseases, in which treatment with extracts of B. dracunculifolia attenuates leukocyte recruitment, tissue edema, oxidative damage, and production of pro-inflammatory cytokines. Finally, B. dracunculifolia is a promising phytotherapeutic resource with potential applications ranging from complementary treatments for inflammatory and oxidative stress-related disorders.
Age-related cognitive impairment is often linked to cholinergic dysfunction and increased oxidative stress. This study explored the neuroprotective potential of lutein–zeaxanthin extract (XanMax ® 2002; LZ) through both in vitro and in vivo approaches. In vitro , Neuro-2a cells exposed to hydrogen peroxide (H 2 O 2 ) were treated with LZ (5–20 μg/mL), leading to decreased expression of apoptosis-related proteins. In vivo , memory impairment was induced by scopolamine in C57BL/6N mice, followed by oral administration of LZ (4 or 8 mg/kg) for 4 weeks. Behavioral assessments—including the Morris water maze, Y-maze, and passive avoidance tests—demonstrated significant improvements in spatial learning, working memory, and memory retention in LZ-treated groups, particularly at the higher dose. Biochemical analysis revealed increased acetylcholine levels, reduced acetylcholinesterase activity, and downregulation of oxidative stress and neuroinflammatory markers in brain tissue. Moreover, LZ supplementation upregulated genes associated with synaptic function and memory. The cognitive-enhancing effects of LZ were comparable with those of donepezil. These findings suggest that LZ may exert neuroprotective effects through antioxidant and anti-inflammatory mechanisms and are a potential dietary intervention for cognitive decline.
Excessive lipid accumulation is a hallmark of metabolic disorders which includes obesity and insulin resistance; however, effective therapeutic strategies remain limited. Tamarixetin (Tx), a naturally occurring flavonoid with diverse pharmacological properties, has not been fully characterized in the context of lipid metabolism. In this study, we explored the metabolic benefits and molecular mechanisms of Tx in a Western diet (WD)-induced obesity model. Transcriptomic profiling revealed that Tx reversed WD-induced gene expression patterns, notably suppressing Pdk4 and inducing Phlda1 expression. Mechanistically, docking analysis suggested that Tx interacts with the acetyl-CoA-binding region within the p300 histone acetyltransferase domain, thereby attenuating H3K9 acetylation at the Pdk4 promoter. This epigenetic inhibition of Pdk4 led to activation of the p38/AMPK signaling cascade, upregulation of PPARGC1A and CPT1A, and enhanced insulin sensitivity in vitro. Collectively, our findings identify Tx as a novel epigenetic modulator that simultaneously suppresses lipogenic gene expression and restores metabolic signaling. Given its natural origin and multifaceted mode of action, Tx emerges as a promising candidate for therapeutic intervention in metabolic disorders.
Dietary restriction of high-protein foods is the primary treatment strategy for phenylketonuria, a disease considered an inborn error of metabolism associated with phenylalanine. The diet of these patients is monotonous, consisting mainly of certain types of fruits and vegetables, and is often supplemented with the use of phenylalanine-free formulas. Considering that Brazil is one of the countries with the most incredible biodiversity in the world, Non-Conventional Food Plants (NCPPs) become food options that can be regularly introduced into the diet of phenylketonuric patients. In the present study, a method for quantifying phenylalanine in NCPPs was validated using high-performance liquid chromatography with an ultraviolet detector. The phenylalanine content was determined in 15 NCPPs samples from the Brazilian Cerrado. The validated method demonstrated selectivity for the amino acid phenylalanine, with linearity in the range of 1-10 nmol/mL, indicating no matrix effect, and provided proven recovery, repeatability, and precision. The detection and quantification limits were 0.0011 mg/100 g and 0.0035 mg/100 g, respectively. The phenylalanine content ranged from 20.28 to 235.58 mg/100 g. It was observed that leafy vegetables had a higher phenylalanine content than the taro stem (20.28 mg/100 g), the chayote fruit (32.67 mg/100 g), the sepal of the sorrel plant (38.21 mg/100 g), and the nasturtium flower (116.24 mg/100 g). These data suggest that these vegetables can be incorporated into the diet of phenylketonuric patients, thereby contributing to dietary diversity and making it less monotonous and more palatable.
Gallic acid, a catechin polyphenol in tea, completely inhibited angiogenesis in assays of human tissue at 10-3 M. Psoriasis is a skin disease caused by excessive secretion of angiogenenic factors by keratinocytes and stromal skin cells. In a double-blind pilot study, six subjects with bilateral plaque psoriasis were treated with 10-2 M gallic acid in a cream base or with a cream base placebo over 8 weeks, four times a day, and treatments were randomly assigned to either the left or the right side. The gallic acid cream was well tolerated, but it did not reduce the psoriasis more than the placebo. One subject wanted to extend treatment for an additional 8 weeks. At the end of 16 weeks, the subject had complete resolution of the psoriatic plaque treated with gallic acid cream. In contrast, the plaque treated with placebo cream was not reduced and stayed equivalent to week six. Gallic acid is inexpensive and does not cause side effects. A longer trial evaluating 10-2 M gallic acid cream for the treatment of psoriasis seems indicated.
Salacia reticulata has long been used in traditional medicine for metabolic disorders, but clinical evidence for obesity-related outcomes remains limited. We conducted a 12-week randomized, double-blind, placebo-controlled trial to evaluate the preliminary efficacy and safety of a standardized Salacia reticulata extract (SLE) on body-fat outcomes. Adults with overweight and/or obesity were randomized to receive SLE capsules or a matching placebo twice daily for 12 weeks. The coprimary endpoints were changes from baseline to week 12 in total body fat mass (g) and body fat percentage (%) measured by dual-energy X-ray absorptiometry. The primary efficacy analysis was conducted in the full analysis set (mITT) using analysis of covariance with baseline values and sex as covariates. Per-protocol set analyses were performed as supportive sensitivity analyses. Among randomized participants, the mITT included 66 participants in the SLE group and 67 in the placebo group, and baseline characteristics were comparable. After 12 weeks, total body fat mass decreased in the SLE group, whereas little change was observed in the placebo group. The between-group difference favored SLE (ANCOVA-adjusted LS mean difference, -482.30 g; 95% CI, -907.05 to -57.54 g). The corresponding between-group comparison was statistically significant (Wilcoxon rank-sum test, P = .0158). Body fat percentage also decreased in the SLE group, but the between-group difference was not statistically significant (ANCOVA-adjusted LS mean difference, -0.30%; 95% CI, -0.73 to 0.12%; Wilcoxon rank-sum test, P = .1453). Several secondary body-composition outcomes, including trunk, android and gynoid fat measures, showed directionally favorable changes in the SLE group. In this 12-week trial, SLE was associated with a modest reduction in total body fat mass, whereas the second coprimary endpoint, body fat percentage, did not differ significantly between groups. These mixed coprimary findings provide only preliminary clinical evidence and should be interpreted with caution, particularly given the study's retrospective trial registration.
Growing interest in hair health has increased the demand for safe and effective hair growth agents. Keratin, a structural protein abundant in hair, skin, and nails, is essential for maintaining hair integrity and resilience. This study evaluated the effects of orally administered hydrolyzed keratin peptide on hair growth in male and female C57BL/6 mice and its cellular impact on human follicle dermal papilla cells (HFDPCs) and HaCaT keratinocytes. Oral administration of hydrolyzed keratin peptide promoted the telogen-to-anagen transition and increased expression of proliferation markers ( β-catenin, cyclin D1 , and proliferating cell nuclear antigen [ PCNA ]) in both sexes, while upregulating growth factors and antioxidant enzymes in male mice. In vitro , hydrolyzed keratin peptide enhanced HFDPC proliferation by activating β-catenin and improving cellular antioxidant capacity in both HaCaT keratinocytes and HFDPCs. These findings suggest that hydrolyzed keratin peptides are a promising functional food ingredient for promoting hair health through both proliferative and antioxidant mechanisms.
Cholestatic liver disease, or cholestasis, is a condition characterized by liver inflammation and fibrosis following a bile duct obstruction and an intrahepatic accumulation of bile acids. Inhibiting inflammation is a promising therapeutic strategy for cholestatic liver diseases. Acer tegmentosum Maxim extract (ATE) is best known for its antiinflammatory and antioxidative properties. In this study, we investigated the effects of ATE on liver injury and fibrosis in mice with bile duct ligation (BDL)-induced cholestasis through analysis of gene expression, cytokines, and histological examination. Oral administration of ATE (20 or 50 mg/kg) for 14 days significantly attenuated hepatocellular necrosis compared to vehicle-treated BDL mice, which was accompanied by the reduced level of serum bile acids and bilirubin. We determined that ATE treatment reduced liver inflammation, oxidative stress, and fibrosis. These beneficial effects of ATE were concurrent with the decreased expression of genes involved in the NF-jB pathway, suggesting that the anti-inflammatory effect of ATE could be a possible mechanism against cholestasis-associated liver injury. Our findings substantiate ATE's role as an alternative therapeutic agent for cholestasis-induced liver injury and fibrosis.
This study compared the immunomodulatory effects of the co-extracted herbal formulation JI-HK601 with those of an individual extracts mixture (IEM) and evaluated the minimum effective dose of JI-HK601 through in vivo immune function analyses in mice. To assess safety, both extracts were administered orally at a dose of 400 mg/kg for 14 consecutive days. Measurements of body weight, spleen index, and peripheral blood cell profiles revealed no significant differences compared to the normal control group, suggesting that neither extract induced systemic toxicity or abnormal immune organ responses under the tested conditions. Immunological assessments indicated that JI-HK601 enhanced natural killer (NK) cell cytotoxic activity to a greater extent than IEM, suggesting a greater functional improvement in NK cell responsiveness. In subsequent dose-response studies of JI-HK601, no toxicity was observed at any dose, whereas increases in T-cell proportion and NK cell activity were noted at 400 mg/kg. Analysis of T-cell transcription factors showed selective upregulation of T-box transcription factor 21 (T-bet), a key regulator of T helper type 1 (Th1) differentiation. These results indicate that JI-HK601 preferentially stimulates Th1-associated immune pathways while enhancing innate cytotoxic function. Overall, the findings demonstrate that JI-HK601 strengthens NK cell activity and promotes Th1-related cellular immunity while maintaining a favorable safety profile across the evaluated dose range. Thus, these results provide foundational data for assessing the potential use of JI-HK601 as an immune-enhancing ingredient in functional foods and complementary and alternative medicine.
This study evaluated the antihyperglycemic effects and mechanisms of Lachnum singerianum polyphenols (LPs) in streptozotocin-induced diabetic mice. LP was obtained via ethanol extraction, purified using XAD-4 resin, and characterized by LC-MS/MS. Diabetic mice were administered low- or high-dose LP (50 or 100 mg/kg), metformin, or their combination for 6 weeks. Metabolic parameters, organ indices, serum and liver biomarkers, histopathology, and signaling pathways were assessed. Liquid chromatography-tandem mass spectrometry (LC-MS/MS) identified LP as flavonoid-, tannin-, and phenolic acid-enriched fractions. LP treatment significantly ameliorated hyperglycemia, as evidenced by reduced fasting blood glucose, improved glucose and insulin tolerance, and restored homeostasis model assessment indices. Furthermore, LP alleviated hepatic injury, attenuated oxidative stress, and ameliorated dyslipidemia, with histopathological analysis confirming protective effects on pancreatic islets and liver tissues. Mechanistically, LP activated the insulin receptor substrate (IRS)/protein kinase B (Akt)/glycogen synthase kinase (GSK)-3β pathway by enhancing IRS-2/Akt phosphorylation and suppressing GSK-3β expression. This is the first study to characterize the bioactive polyphenols from L. singerianum and demonstrate their multitarget efficacy against diabetic hyperglycemia through coordinated modulation of insulin resistance, oxidative stress, and lipid metabolism.
Bromelain is a mixture of enzymes found in several parts of the pineapple plant, including the stem, fruit, leaves, and peel. Its use was recommended to slow down the progression of neurological disorders such as Parkinson's disease. Although studies have examined the beneficial effects of bromelain (Br) in neurological disorders, its detailed benefits in schizophrenia are still poorly understood. We, thus, modeled schizophrenia using two developmental methods. In the first experiment, postweaning social isolation (SI) method where male mice were weaned at postnatal day (PND) 21 and isolated in individual cage for 5 weeks was used to induce schizophrenia. The second experiment used a maternal deprivation (MD) model, where mothers were separated from their pups for 24 h at PND 9. In both experiments 1 and 2, Br was administered orally from PND 21 to PND 56. At PND 56, there were behavioral assessments of nest building, anxiety, depression, and locomotion, while oxidative stress, neuroinflammation, brain-derived neurotrophic factor, and astrocyte expression in the prefrontal cortex and hippocampus were assessed at the end of the behavioral studies. Our study found that both SI and MD caused anxiety, depression, and hyperlocomotion. This was accompanied by oxidative stress in the prefrontal cortex and hippocampus, and neuroinflammation was observed only in the hippocampus. While SI rearing caused poor nest-building capacity, MD rearing did not impact nest-building capacity of the mice. The study found that administration of 50 mg/kg of Br reversed oxidative stress and neuroinflammation and significantly reduced anxiety level, hyperlocomotion, and depression in the mice. Mice administered Br also had a better nest-building capacity. Br may, therefore, benefit individuals at ultra-high risk and patients with schizophrenia, alleviating the positive, negative, and cognitive symptoms of the disease, without the side effects reported in the use of psychotic drugs.
Chronic kidney disease (CKD) is a systemic condition associated with inflammation and oxidative stress, affecting organs beyond the kidneys. Although rarely emphasized, the eyes may also be affected but underlying molecular mechanisms remain largely unexplored. The gut-kidney and gut-eye axes are emerging as therapeutic targets with prebiotics like ResistAid®-a Larch Arabinogalactan (LAG) supplement with antioxidant and immunomodulatory effects-showing promise through gut microbiota modulation. This study assessed ResistAid®'s effects on ocular gene expression in a CKD rat model. Twenty four Wistar rats were assigned to Sham (S), Sham + Treatment (ST), Nephrectomized (N), Nephrectomized + Treatment (NT) (n = 6 each). CKD was induced by 5/6 nephrectomy. The treatment was administered via gavage for 30 days at a dose of 5.35 mg/day, adapted from human recommendations. At day 30, blood and tissues were collected. Expression of antioxidant enzymes (Cat, Sod1, Gpx1, Gpx4) and other genes (Nfe2l2, Nfκb1, Timp3, Hif-1α, Kim1, Klotho) was analyzed by qPCR. Biochemical and well-being assessments were also conducted. Nephrectomy, regardless of treatment, increased Sod1 and Hif1ɑ expression in eye and blood; Specific to NT animals, ocular Gpx1, Gpx4 and Nfe2l2 expressions were markedly elevated when compared with N animals and blood Kim1 and ocular Nfκb1 expressions were not elevated, differing from N animals. No significant changes were observed between the S and ST groups. CKD induces systemic oxidative and inflammatory responses. ResistAid® partially mitigated these effects in blood and eye, suggesting systemic and local benefits, possibly via gut microbiota modulation.
This study investigated the effects of nasal inhalation of Osmanthus fragrans var. aurantiacus (OFA) extract in lipopolysaccharide (LPS)-challenged rats. Electronic nose analysis of the OFA extracts identified 25 volatile organic compounds. Gas chromatography-mass spectrometry-olfactometry (GC-MS-O) analysis revealed that β-ionone, linalool, and related derivatives are the primary odor-active compounds in the OFA extract. LPS exposure increased pro-inflammatory markers like tumor necrosis factor-alpha, caused organ hypertrophy in the liver, lungs, and spleen, and altered transcriptional profiles linked to nuclear factor-kappa B (NF-κΒ) and immune pathways. RNA sequencing of brain tissues showed that while LPS strongly elevated NF-κΒ and cytokine pathways, this effect was less pronounced in OFA-treated rats, indicating reduced LPS-driven inflammation at the transcriptome level. Overall, these findings highlight the potential of OFA extract, abundant in β-ionone and linalool, to mitigate inflammatory signaling and improve select metabolic markers in an LPS-induced inflammatory model.
Melphalan, a widely used alkylating chemotherapeutic agent, is known to cause gonadotoxicity, particularly affecting spermatogenesis and steroidogenesis. This study investigated the protective effects of chrysin, a flavonoid with antioxidant and antiapoptotic properties, on melphalan-induced testicular damage in immature male rats. Forty-eight prepubertal Wistar rats were divided into six groups receiving melphalan (0.5 mg/kg/day, intraperitoneally), chrysin (50 or 75 mg/kg/day, orally), or combinations thereof. Treatment spanned 30 days, covering the prepubertal to pubertal transition. Melphalan exposure significantly reduced testosterone levels, disrupted spermatogenesis, and increased oxidative stress, as indicated by elevated malondialdehyde and decreased glutathione peroxidase levels. Gene expression analysis revealed marked upregulation of autophagy (LC3β, Beclin-1, Atg5, Atg7, Atg12) and apoptosis (BAX, caspase-3) markers, alongside downregulation of the antiapoptotic gene BCL2. Histological analysis showed severe damage to seminiferous tubules and reduced Johnsen scores. Chrysin coadministration, particularly at 75 mg/kg, significantly ameliorated these effects by restoring antioxidant capacity, reducing expression of cell death-related genes, and improving testicular structure and hormone levels. These findings demonstrate that chrysin mitigates melphalan-induced gonadotoxicity through modulation of oxidative stress, apoptosis, and autophagy pathways. Chrysin's dose-dependent protective effects highlight its potential as a natural therapeutic agent to preserve reproductive function in individuals undergoing chemotherapy during prepuberty.
Osteoarthritis (OA) is characterized by inflammation-driven chondrocyte senescence and extracellular-matrix degradation. However, the molecular mechanisms linking inflammatory stress to chondrocyte aging remain poorly understood. Here, we identify cinnamyl alcohol (CA) as a natural small-molecule compound that attenuates OA progression through polymeric immunoglobulin receptor (PIGR)-mediated signaling in vitro. CA reduced inflammatory cytokine production, suppressed senescence-associated secretory phenotype gene expression, and preserved cartilage homeostasis in lipopolysaccharide- or interleukin-1β-stimulated chondrocytes. In a destabilization-of-the-medial-meniscus mouse model, intra-articular CA administration markedly alleviated cartilage degeneration and matrix loss. Integrating network pharmacology, molecular docking, and mass-spectrometry-based proteomic profiling, we identified PIGR as a convergent target of CA, validated by limited proteolysis (drug affinity responsive target stability) and loss-of-function assays. PIGR silencing abolished CA's antisenescent and cartilage-protective effects, confirming its essential role. Mechanistically, CA restored PIGR expression to modulate inflammatory signaling and maintain chondrocyte phenotype stability. These findings uncover a previously unrecognized CA-PIGR axis that couples inflammatory stress to cartilage aging and suggest CA as a promising natural therapeutic candidate for OA management.
Hypercholesterolemia is a major risk factor for cardiovascular disease, necessitating the development of effective and safe lipid-lowering interventions. This study evaluated the antihypercholesterolemic effects of KGC11o, a red ginseng oil obtained via supercritical fluid extraction, using both HepG2 cells and a high-fat/high-cholesterol diet-induced hypercholesterolemic rat model. KGC11o treatment significantly improved serum and hepatic lipid profiles, reduced markers of liver injury, and enhanced fecal cholesterol excretion. At the molecular level, KGC11o modulated the expression of key genes involved in cholesterol biosynthesis (3-hydroxy-3-methylglutaryl-CoA reductase), esterification (acyl-CoA:cholesterol acyltransferase), transport (CETP, LPL), and catabolism (LCAT, cholesterol 7α-hydroxylase). Collectively, these findings suggest that KGC11o may serve as a safe, food-derived functional ingredient with potential benefits for the management of hypercholesterolemia and related metabolic disorders. Further studies are warranted to elucidate its molecular mechanisms and to confirm its clinical efficacy.
This study was conducted to determine the effects of fructo-oligosaccharide (FOS) inulin on anxiety symptoms in college students. Forty million adults in the United States suffer from anxiety. Previous studies have viewed gut microbiota and its potential link to anxiety in both humans and mice. However, no previous studies focused on the effect of FOS inulin on college students. Fourteen subjects received 4.9 g per day of FOS inulin as the treatment (TX) or no supplement as the control (CON) for 28 days. Both the TX and CON groups were given the Generalized Anxiety Disorder 7-Item Scale (GAD-7) on days 1 and 28. Both groups were also given a 3-day food log at the beginning of the experiment and otherwise maintained their regular diet. Results showed a statistically significant decrease in median GAD-7 scores in both groups (P = .017, r = .637 and P = .042, r = .587 for the TX and CON groups, respectively). However, when comparing the GAD-7 scores between groups, no statistically significant results were found. FOS inulin supplementation did not alleviate anxiety symptoms in college students participating in this study.
