Journal of medicinal food最新文献

Diabetes, considered one of the main causes of death in the Mexican population, is a chronic disease caused by alterations in the synthesis of pancreatic insulin or because it is not used effectively by the body. Insufficient action of insulin causes hyperglycemia, which, if not controlled, causes damage to blood capillaries and nerve endings over time, affecting the functioning of various organs and systems. As mentioned above, controlling glucose levels in the population suffering from chronic diseases becomes an essential part of their treatment. The aim of this study was to evaluate the hypoglycemic effect of a hydroalcoholic extract of the aerial parts of Porophyllum ruderale (HEPr). A glucose tolerance curve was developed by monitoring at different times (0-120 min) glucose levels in blood samples taken from an apical tail slice of CD1 mice. HEPr showed a significant effect from baseline on basal glucose levels (114.33 ± 14.74 mg/dL) compared with the control group (60.33 ± 4.16 mg/dL) and the metformin-treated group (129 ± 13 mg/dL). In addition, the values at the end of the tolerance curve (120 min) showed a significant decrease in the study group (66 ± 10.39 mg/dL) compared with the metformin-treated group (108.67 ± 4.50 mg/dL). This effect can be attributed to the presence of chlorogenic acid, cryptochlorogenic acid, ferulic acid, quercetin, and kaempferol 3-O-glucosides in HEPr. In conclusion, P. ruderale constitutes an important source of compounds for use as an adjuvant treatment for the control of hypoglycemia in different chronic diseases.

Fubai chrysanthemum is a kind of traditional Chinese medicine, which can be used as a common food, and is commonly used to improve and relieve visual fatigue. However, its pharmacodynamic material basis and action mechanisms in relieving visual fatigue have not been systematically studied. In this article, 11 absorbed ingredients from Fubai chrysanthemum were detected in rat plasma. Then, the target network pharmacology and KEGG pathway analysis were performed. It was found that Fubai chrysanthemum could inhibit various apoptotic cells and reduce oxidative damage of eyes by regulating the apoptosis pathway, thus alleviating visual fatigue. Further in vitro experiments showed that Fubai chrysanthemum could effectively protect against oxidation damage of adult retinal pigment epithelial cells (ARPE-19), retinal ganglion cells (RGC-5), and lens. The results of cell experiments showed that Fubai chrysanthemum could increase the cell activity, GSH content, and SOD content of ARPE-19 and RGC-5 after oxidative injury, while decreasing the IL-18 content. Similarly, in the study of lens transparency, we found that Fubai chrysanthemum could effectively alleviate the oxidative damage degree of the lens, and significantly increase the content of CAT, GSH, and SOD. The above results suggested that Fubai chrysanthemum could play an important role in alleviating visual fatigue through regulating cell apoptosis and antioxidative damage.

Saxidomus purpurata extract (SPE) is a highly consumable seafood worldwide with known health-related benefits. However, there are no reports of its' anti-obesity effect. This study explores the potential of SPE for anti-obesity effects by modulating adipogenesis and lipolysis. SPE reduced intracellular lipid and triglyceride accumulation while increasing free glycerol release in adipocytes. SPE inhibited lipogenesis protein expressions and increased the phosphorylation of hormone-sensitive lipase and Adenosine monophosphate-activated protein kinase (AMPK) to promote lipolysis. In addition, SPE suppressed adipogenesis by downregulating protein expression of key adipogenic markers, peroxisome proliferator-activated receptor gamma (PPARγ), CCAAT/enhancer-binding protein α (C/EBPα), and sterol regulatory element-binding protein 1 (SREBP1) via Wnt/β-catenin signaling. SPE augmented the heme oxygenase-1 (HO-1) expression. Thus, pharmacological intervention with Zinc protoporphyrin (ZnPP-HO-1 antagonist) was employed to validate the HO-1 role. The presence of ZnPP increased the lipid accumulation and reduced the free glycerol release. At the molecular level, adipogenic transcription factors (PPARγ, C/EBPα, and SREBP1) expressions were restored in the presence of ZnPP. GC-MS analysis revealed that SPE was comprised of several fatty acids, contributing to its anti-obesity activity. SPE is an effective nutraceutical that can be used to reduce the progression of obesity. HO-1 expression during adipogenesis might be the mechanism of action for the anti-obesity effect of SPE.

Several rural Moroccan people depend on natural remedies such as Smen (ghee) before visiting a health center due to their low cost and accessibility. However, knowledge of Smen traditional medicine is not documented but rather transferred orally from generation to generation. This is the first qualitative ethnomedicinal study that provides and documents information about the medicinal use of Smen in Northern Morocco. The present study aimed to investigate and gather information on the traditional medicinal practices of using Smen among rural people in Northern Morocco for a document and suggest the exploration of this product and its bioactive compounds in medical applications. The investigation was carried out by conducting individual semistructured interviews with 630 elderly people from March to April 2022. Data were analyzed using descriptive statistics and expressed as a percentage of responses to each question in the survey. The study revealed that 66.5% of the people surveyed were aware of the medical benefits of Smen, which had been passed down from their ancestors. It has been used to treat hemorrhoids, common colds, detoxification, rheumatism, and wound/burn injuries. This study showed that Moroccan's ethnomedicinal knowledge is closely related to Ayurveda, ancient Indian traditional medicine. For centuries, Smen has been used traditionally for medical purposes, just as it has been used in cooking. The diversity of ghee medicinal use in Northern Morocco could contribute to the discovery and development of ghee-based drugs, which have fewer side effects.

In numerous countries, the utilization of plants for both nutritional and therapeutic purposes is a common practice. However, the inadvertent use of these plants can pose risks due to their active molecules or microbiota. The traditional use of Herniaria glabra L. (H. glabra) plant in treating various diseases is well-known; however, its application in yogurt production raises concerns. In this study, Bacillus pumilus isolated from H. glabra was identified through 16s rRNA sequencing and MALDI-TOF MS (Matriks Assisted Lazer Desorption Ionization Time of Flight Massspectrometry). The bacterium's resistance under simulated gastrointestinal tract (GIT) conditions was assessed, followed by investigations into its aggregation ability, antibiotic resistance, hemolytic activity, and antagonistic potential through in vitro tests. The study revealed that B. pumilus exhibited 100% resistance to GIT conditions. Notably, the bacterium demonstrated strong autoaggregation (34.48%) and coaggregation abilities (49.82% for Escherichia coli, 49.13% for Listeria monocytogenes), signifying a potent aggregative potential. Sensitivity to most tested antibiotics was observed, while no antagonistic activity against tested bacteria was evident. Furthermore, the bacterium exhibited β-hemolytic activity, indicative of potential virulence. The findings suggest that this resistant yet virulent bacterium, with its hemolytic activity, could disrupt the GIT balance, posing serious health risks. The study underscores the need for caution and awareness regarding the potential dangers posed by bacteria in plant microbiota in herbal therapies.

Acrylamide (ACR) is an obligate human neurotoxicant ubiquitously produced and found in foods processed at high temperature. There is an increasing public health concern regarding its probable carcinogenic potential. Its prevailing toxicity mechanism is oxidative inflammation and apoptosis. Herein, we explored whether thymoquinone (TQ), a bioactive quinone in Nigella sativa seed, could mitigate ACR-induced cerebellar toxicity in rats. Our study design featured four rat groups: control, TQ (5 mg/kg bw), ACR (50 mg/kg bw), and TQ + ACR (5 mg/kg + 50 mg/kg). After 14 days of respective treatments, cerebellar homogenate was used to estimate acetylcholinesterase activity (AchE) activity, antioxidant enzymes (catalase [CAT], superoxide dismutase [SOD], and glutathione peroxidase [GPx]), malondialdehyde (MDA), inflammatory cytokines (interleukin [IL]-6, tumor necrosis factor [TNF]-α, IL-4, and IL-10), nuclear factor kappa B (NF-κB), nuclear factor erythroid 2-related factor 2 (Nrf2), caspase-3, and caspase-9. The level of DNA damage by fragmentation and histopathological lesions was also determined in the cerebellum. The rat exposure to ACR caused significant decreases in the cerebellar activities of AchE, CAT, SOD, and GPx, IL-4, IL-10, and expression of Nrf2, whereas the levels of MDA, IL-6, TNF-α, caspase-3, and caspase-9 were prominently increased compared with the control. ACR induced significant DNA fragments and cerebellar lesions when compared with the control. Contrarily, TQ treatment inhibited the depression of CAT, SOD, and GPx activities and reversed the MDA level and expression of Nrf2/NF-κB, cytokines, and caspases. These effects were confirmed by reduced DNA damage and cerebellar histopathological lesions in comparison with the ACR. TQ afforded neuroprotection via its antioxidant, anti-inflammatory, and antiapoptotic mechanisms in rats.

Gulf War Illness (GWI) afflicts US military personnel who served in the Persian Gulf War. Suspect causal agents include exposure to pyridostigmine (PB), permethrin (PM) and N,N-diethyl-m-toluamide (DEET). Prominent symptoms include cognitive deficits, such as memory impairment. In aging animal models, we have documented the beneficial effect of the flavanol (-)-epicatechin (Epi) on hippocampus structure and related function. Using a rat model of GWI, we examined the effects of Epi on hippocampus inflammation, oxidative stress, mitochondrial dysfunction, cell death/survival pathways, and memory endpoints. Male Wistar rats underwent 3 weeks of exposure to either vehicles or DEET, PM, PB, and stress. Subgroups of GWI rats were then allocated to receive orally 15 days of either water (vehicle) or 1 mg/kg/day of Epi treatment. Object recognition tasks were performed to assess memory. Hippocampus samples were analyzed. Epi treatment yields significant improvements in short- and long-term memory versus GWI rats. Hippocampus oxidative stress and pro-inflammatory cytokine levels showed significant increases with GWI that were largely normalized with Epi becoming comparable to controls. Significant increases in markers of hippocampus neuroinflammation and cell death were noted with GWI and were also largely reduced with Epi. Neuronal survival signaling pathways were adversely impacted by GWI and were partially or fully restored by Epi. Markers of mitochondrial function were adversely impacted by GWI and were fully restored by Epi. In conclusion, in an animal model of GWI, Epi beneficially impacts recognized markers of hippocampus neuroinflammation, oxidative stress, cell survival, neurotoxicity and mitochondrial function leading to improved memory.

Our aim in the current study was to determine the in vitro and in vivo synergistic antiinflammatory and antiallergic effect associated with the IL-12 production of guaijaverin and epigallocatechin gallate (EGCG) complex (GEC) and ILS-F-2301 (2:8 extract of Psidium guajava and Camellia sinensis). Compared to EGCG alone, GEC showed synergistic inhibition of nitric oxide (NO), inducible NO synthase, and cyclooxygenase-2 by 3.8, 5.1, and 4.1%, respectively. The downregulation of interleukin-12 (IL-12) by 2,4-dinitrophenyl-human serum albumin conjugate/DNP-immunoglobulin E or ovalbumin (OVA) was synergistically increased by GEC by about 7.5% or 5.4% compared to EGCG alone. The level of downregulation of IL-12 in plasma increased by 100 mg/kg with ILS-F-2301 (28.7%) when compared to the OVA/Alu-treated group. Also, GEC synergistically increased by GEC by about 7.5% or 5.4% compared to EGCG alone. The level of down and cyclooxygenase C synergistically inhibited p-Akt, PI3K, mTOR, p-STAT6, and GATA3 by 4.9%, 4.1%, 19.2%, 23.8%, and 35.3%, respectively, while increasing the expressions of p-STAT1 and T-bet (showing 53.3% and 9.4% activation) when compared to EGCG alone. In an allergenic rhinitis mouse model, 100 mg/kg of ILS-F-2301 was shown to inhibit p-Akt, PI3K, mTOR, p-c-Jun N-terminal kinase (p-JNK), p-extracellular signal-regulated kinase (p-ERK), and p-p38 by 23.3%, 43.8%, 17.2%, 32.2%, 29.1%, and 41.8% when compared to the OVA/Alu-sensitized group. Taken together, our findings suggest that ILS-F-2301 may have potential as a functional food for alleviating antiallergic rhinitis.

Excessive and prolonged alcohol consumption can lead to a serious health condition known as alcohol-related liver disease (ARLD). This ailment represents a significant worldwide health challenge, affecting populations across various demographics. ARLD has a multifactorial pathogenesis involving oxidative stress, inflammation, dysregulated lipid metabolism, and apoptosis. In this study, we investigated the hepatoprotective effects of Laurus nobilis L. leaf water extract (LLE) against ARLD in alcohol-treated hepatocytes and mice. LLE exhibited antioxidant and anti-inflammatory properties by enhancing antioxidant enzyme activities and suppressing proinflammatory cytokines and CYP2E1 expression in ethanol-treated hepatocytes. Moreover, LLE mitigated lipogenesis by modulating the expression of lipogenic factors in ethanol-treated hepatocytes. In vivo, LLE administration attenuated liver injury, oxidative stress, inflammation, and lipid accumulation induced by alcohol consumption in mice. Additionally, LLE suppressed apoptosis signaling pathways implicated in alcohol-induced hepatocyte apoptosis. These findings suggest that LLE functions as a multifaceted therapeutic agent for ARLD by modulating multiple cellular mechanisms, including the reduction of oxidative damage, mitigation of inflammatory responses, alleviation of lipid-mediated toxicity, and regulation of programmed cell death pathways.