Journal of medicinal food最新文献

Glycogen storage diseases are genetic disorders involving glycogen storage or release. The cost of the modified starch (trademark Glycosade®) for treatment sometimes is not feasible, and patients are treated with oral uncooked cornstarch every 3 h. Our aim was to modify cornstarch at the lab and to translate it to a homemade process to extend glucose uptake for at least 5 h. We measured the transition phase of available cornstarch at low moisture. Then, cornstarch was heat-treated in a laboratory convection oven at 90, 95, and 100°C for 2 and 5 h and analyzed for in vitro hydrolysis and digestibility in comparison to Glycosade® by a cluster analysis. We replicated conditions in a kitchen roasting oven. A trial with 19 fasted healthy adults evaluated glucose after intake of 100 g/300 mL for 5 h. There were no phase transitions at 30% moisture, up to 100°C. At the lab, optimum conditions were 5 h at 90°C, with similar in vitro behavior to Glycosade®, and 95°C for 2 h in the kitchen roasting oven. The glucose levels of participants were maintained (106 to 95 mg/dL) along 5 h. In conclusion, euglycemia was prolonged at least 5 h after our product dosing as breakfast. The modified cornstarch could be prepared at home and used in patients with glycogen storage diseases, after clinical assessment.

Type 2 diabetes mellitus (T2DM), characterized by progressive insulin secretion defect based on insulin resistance, is one of the leading public health problems with high morbidity and mortality rates. Uncontrolled hyperglycemia, which becomes a more severe indication with obesity in T2DM patients, increases the risk of cardiovascular disease, kidney damage, and retinal disorder. Effective diabetes treatment is possible with a comprehensive approach that includes controlling blood glucose levels, improving pancreatic β cell functions, and supporting insulin sensitivity through body weight management, nutritional therapy, and drug therapy. At this point, food-derived bioactive peptides and protein hydrolysates, which draw attention with their structural similarity to regulatory peptides in human metabolism, have great potential in treating T2DM and regulating glucose metabolism. Various glucoregulatory properties of bioactive peptides come to the fore through antidiabetic mechanisms such as the digestion of carbohydrates, the release of intestinal hormones, insulin function and secretion, glucose uptake, and adipose tissue modification. This review aims to evaluate the roles of food-derived bioactive peptides and protein hydrolysates in controlling glycemia and insulin sensitivity and their antidiabetic mechanisms of action and to examine the difficulties and opportunities related to the acquisition and research processes.

Beetroot has been traditionally used in folk medicine to treat various gastrointestinal disorders and is commonly consumed for its high antioxidant content. The primary objective of this study is to demonstrate, for the first time, the potential therapeutic effects of beetroot juice (BJ) in a rat model suffering from ulcerative colitis (UC) induced by dextran sulfate sodium (DSS). In addition, the study aims to identify the bioactive compounds in beetroot responsible for these effects. UC was induced in rats through the oral administration of DSS dissolved in drinking water (5%) during the final week of a 21-day treatment with BJ (5 and 10 mL/kg body weight) and compared to a reference drug, mesalazine. Phytochemical analysis revealed that BJ is a rich source of secondary metabolites such as polyphenols, flavonoids, soluble sugars, and betalains. The pretreatment with BJ significantly and dose-dependently reduced DSS-induced colonic mucosa lesions and associated histopathological alterations. The protective effects of BJ on the colonic mucosa were closely linked to its ability to mitigate oxidative damage, inflammatory injury, and biochemical imbalances. Specifically, BJ counteracted DSS-induced lipid peroxidation and restored levels of both enzymatic and nonenzymatic antioxidants. Moreover, BJ significantly decreased the levels of inflammatory markers and cytokines in plasma and colonic mucosa, while enhancing plasma scavenging activity and maintaining the homeostasis of intracellular mediators such as hydrogen peroxide, free iron, and ionizable calcium. These findings supported the use of BJ as a complementary approach for managing UC and underscore the need for further investigation into its potential clinical applications.

Cyclosporine A (CsA) is a powerful immunosuppressant drug most widely used in managing organ transplantation and autoimmune diseases. The aim of this work was to investigate the role of taurine in alleviating the apoptotic hepatocytes and oxidative stress caused by CsA in rats' livers. The four experimental groups were evaluated, including (GpI) vehicle control (olive oil), (GpII) Tau (5 mg/kg/day), (GpIII) CsA (50 mg/kg/day), and (GpIV) CsA + Tau. The biochemical assay in liver functions and antioxidant enzymes was assayed, and the histopathology of hepatic tissue and immunohistochemical staining of apoptotic protein (p53) and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) were determined. Induction of CsA in rats caused severe hepatotoxicity, as evidenced by the elevation of serum aspartate aminotransferase, alanine aminotransferase activities, and alkaline phosphatase concentration and decreased catalase (CAT), glutathione peroxidase, and glutathione reductase activities. The histopathological examination revealed mild to marked disorganization in the liver tissue, characterized by hepatocyte degeneration/necrosis, apoptotic hepatocytes, sinusoidal dilatation, and inflammatory cell infiltration. Whereas Tau treatment improved the liver function enzymes and increased the oxidative stress by elevating the antioxidant enzyme CAT and glutathione reductase. There is recovery of destructive liver tissue preserved hepatic trabecular architecture; dark nuclei with prominent nucleoli, hepatocytes, and mild dilated sinusoids; small area of pyknotic hepatocytes have vacuolated cytoplasm was seen, and the number of apoptotic cells detected by TUNEL and p53 protein was significantly decreased (P = .001). The results may contribute to the hepatoprotective role of Tau and its ability to ameliorate the oxidative stress and alleviate the apoptotic hepatocytes induced by CsA. So, Tau may have had a beneficial role in reducing tissue damage in patients exposed to CsA.

Although probiotic products are widely used to promote gut health, their long-term efficacy is often constrained by poor colonization and transient microbial modulation. To address these limitations, we developed and evaluated a probiotic beverage comprising Lactobacillus-based strains (Lactobacillus rhamnosus LGD-0817, L. rhamnosus LDL-1708, Lactobacillus casei LPM-0188, Lactiplantibacillus plantarum LEP-1208, Lactobacillus delbrueckii subsp. bulgaricus RHM-1068, Lactobacillus paracasei LPA-2088, L. paracasei BMC-2020, Limosilactobacillus fermentum LAF-1387, and L. plantarum MCA-3066) formulated to optimize inter-strain synergy, enhance colonization efficiency, and improve long-term functionality. 16S rRNA sequencing conducted one week after treatment cessation revealed a marked enrichment of Lactobacillales and Lactobacillaceae-taxonomic groups to which administered probiotic strains belong-indicating durable colonization by the introduced strains. To further assess the functional relevance of this microbial shift, a dextran sulfate sodium-induced colitis model was employed. Probiotic intervention significantly improved disease outcomes, including increased colon length, reduced histopathological inflammation scores, enhanced goblet cell numbers, and lowered levels of pro-inflammatory cytokines (IL-6, Tumor Necrosis Factor-alpha (TNF-α), and Interleukin (IL)-1β). Collectively, these results underscore the efficacy of this formulation in achieving sustained modulation of the gut microbiota and alleviating intestinal inflammation, and support its potential for broader applications in gut health management.

Eriobotrya japonica, a Rosaceae family plant, is cultivated in East Asia and possesses various biological activities. It has a long history of use in traditional medicine practices. Benign prostatic hyperplasia (BPH) is a common urological issue in aging men. Although its exact etiology remains unidentified, it is believed to be caused by a combination of factors such as aging, inflammation, and hormonal imbalance. This study examined the effects of E. japonica leaf 50% ethanol extracts (EJE) on human prostate epithelial BPH-1 cells and a BPH rat model developed via testosterone propionate (TP) injection. In BPH-1 cells, EJE treatment suppressed the proliferation of the cells in a dose-response relationship. In addition, mRNA expression levels of androgen receptor (AR), steroid 5 alpha-reductase type 2 (SRD5A2), and Bcl-2 were decreased, and Bax expression and the Bax/Bcl-2 ratio were increased by EJE treatment. In the in vivo experiment, castrated Sprague-Dawley (SD) rats were orally administered EJE at the following doses: 50-200 mg/kg of body mass. EJE administration reduced prostate weight, prostate ratio, serum dihydrotestosterone (DHT) levels, and serum testosterone levels. It also decreased intraprostatic DHT levels and 5α-reductase 2 expression. Histological analysis revealed a reduced epithelial thickness and increased lumen area in the EJE treatment group. Furthermore, the expression of AR, Bcl-2, tumor necrosis factor (TNF)-α, interleukin (IL)-8, IL-6, IL-1β, and cyclooxygenase-2 (COX-2) in prostate tissues was lowered by EJE administration. In conclusion, EJE effectively alleviated benign prostatic hyperplasia, both in cells and in animal models, by regulating inflammation, suggesting it is a potential candidate as a functional ingredient for alleviating BPH.

The antibacterial effect of chloramphenicol, hibiscus acid, and a mixture of hibiscus acid and chloramphenicol against antibiotic-resistant enterohemorrhagic Escherichia coli (EHEC) and Salmonella Typhimurium (ST) was determined in Caesarean-Derived (CD)-1 mice. Hibiscus acid was isolated from Hibiscus sabdariffa calyces. The minimum inhibitory concentration (MIC) and the minimum bactericidal concentration (MBC) of chloramphenicol (CH), hibiscus acid (HA), and mixtures of HA/CH were determined for EHEC and ST. 11 groups of six mice each were formed. Four groups were inoculated orally with 4 log₁₀ Colony forming units (CFU) of ST, four groups were inoculated with 4 log₁₀ CFU of EHEC, and the remaining three groups were not inoculated. Six hours post inoculation, the mice in some groups received, via the oral route, solutions of hibiscus acid (7 mg/mL), chloramphenicol (82 µg/mL), a mixture of HA/CH (5.7 mg/mL HA and 4 µg/mL CH), or isotonic saline solution. The MIC and MBC values were between 7 and 5 mg/mL for hibiscus acid, between 17.6 and 82 µg/mL for chloramphenicol, and between 4.2 mg/mL/0.3 µg/mL and 5.7 mg/mL/0.4 µg/mL (concentration of hibiscus acid/concentration of chloramphenicol) or HA/CH. EHEC and ST were not detected in the feces of mice that were administered hibiscus acid alone or in mixture with chloramphenicol. By contrast, pathogens were isolated from the feces of untreated mice and those treated with chloramphenicol alone throughout the study.

Acute lung injury (ALI), primarily triggered by bacterial infection, occurs via intricate immune defense mechanisms within the lungs. This study aimed to investigate the potential of Craibiodendron stellatum (Pierre) WW Sm. extract (CSE) as an anti-inflammatory agent in a lipopolysaccharide (LPS)-induced C57BL/6 mouse ALI model and RAW 264.7 macrophages. Results showed that oral CSE administration significantly suppressed LPS-induced ALI symptoms, including hemorrhage in alveolar spaces, thickened alveolar walls, and inflammatory cell infiltration; it also inhibited the production of proinflammatory cytokines in the lungs. Additionally, oral CSE administration attenuated the LPS-induced iNOS expression in mouse lungs. CSE also inhibited the LPS-induced nuclear factor-kappa B signaling in RAW 264.7 cells. DCF-DA assay confirmed that CSE could reduce the LPS-induced reactive oxygen species production. Our findings suggested that CSE may be useful as a functional respiratory health material by regulating the inflammatory signaling pathway in alveolar macrophages in ALI induced by bacterial infections.

Isoliquiritigenin (ISL), a bioactive phytochemical derived from the root of Glycyrrhiza uralensis, is known to exert anticancer effects by modulating cancer cell functions, including proliferation, metastasis, and autophagy. However, the anticancer effects of ISL on cholangiocarcinoma (CCA) are limited. In this study, we investigated the anticancer effects of ISL on CCA cells (SNU-478 and HuCCT-1). In SNU-478 cells, ISL decreased the expression of glucose-regulated protein 78 (GRP78). ISL was also found to significantly reduce cell viability and colony area of both SNU-478 and HuCCT-1 cells. Furthermore, ISL treatment significantly increased the population of apoptotic cells, as observed through Annexin V/propidium iodide (PI) staining. PI staining showed that the ISL treatment induced significant cell cycle arrest compared to the control group, indicating that ISL-induced decreases in cell viability are associated with cell cycle arrest and apoptosis. ISL treatment also resulted in a significant decline in the mitochondrial membrane potential when observed through JC-10 staining. Mitochondrial superoxide staining revealed that ISL significantly upregulated the generation of mitochondrial reactive oxygen species (ROS). Acridine orange staining indicated that the ISL treatment upregulated lysosomal membrane permeability, which could be related to autophagy. These results suggest that ISL affects the proliferation and apoptosis of CCA cells, which might be related to its regulatory role in various cellular functions, including mitochondrial dysfunction, ROS balance, and autophagy. This study provides empirical evidence that ISL could be a potential candidate for CCA therapy.

The aim of this study was to determine the effects of microencapsulated and nonencapsulated aronia (Aronia melanocarpa) extract on paraoxonase 1 (PON1) mRNA expression, HDL cholesterol, and aortic atherosclerosis in rat blood and liver tissues. The study involved 42 male Sprague-Dawley rats aged 10 weeks. The experimental groups were as follows: (1) standard diet control (CON), (2) high-fat diet (HF) control, (3) HF + 400 mg/kg aronia extract (HF400E), (4) HF + 200 mg/kg aronia extract (HF200E), (5) HF + 400 mg/kg microencapsulated aronia (HF400C), and (6) HF + 200 mg/kg microencapsulated aronia (HF200C). The rats were fed a HF between the 10th and 20th week, and at the end of the 20th week, all groups except CON were administered aronia extract (200-400 mg/kg) by oral gavage for 6 weeks. After 6 weeks, biochemical analyses and aortic histology evaluations were performed. The results showed that the HF significantly increased serum total cholesterol, triglycerides, low-density lipoprotein levels, and hepatic malondialdehyde levels. However, administration of HF400E significantly reduced these parameters in hyperlipidemic rats. Serum PON1 enzyme activity was significantly higher in the HF400E group compared with both the CON (P < .001) and HF (P < .0025) groups. Although PON1 mRNA levels in the HF400E, HF200E, and HF200C groups were higher than in the CON and HF groups, the differences were not statistically significant. Evaluation of the aortic tissues showed normal tissue morphology in all experimental groups, with no signs of atherosclerotic plaques, hyaline or mucoid changes, or endothelial anomalies in the thoracic or aortic arch tissues. These findings suggest that aronia, rich in anthocyanins and other polyphenolic compounds, may help prevent and slow down atherosclerosis by enhancing PON1 enzyme activity, which is involved in preventing lipid oxidation, the first step in atherosclerosis.