Advances in Traditional Medicine最新文献

Tripterygium wilfordii Hook. f. (TWHF) is a traditional Chinese medicine with multiple pharmacological activities, yet its therapeutic effects on type I hypersensitivity has not been clarified. This study investigated the treatment and potential mechanisms of TWHF and its major bioactive component Triptolide (TPL) on type I allergy. The treatment mechanism was predicted by network pharmacology. Tripterygium wilfordii Polycoride Tablet (TWPT) and TPL were selected as therapeutic agents for type I allergy in RBL-2H3 cell and in PCA and PSA models.25 molecular targets were screened, and IL4, IL2, PIK3CG and CXCR4 that have a strong correlation with TWHF anti-type I allergy. Furthermore, TWHF may regulate type I allergy via Th1 and Th2 cell differentiation, PI3K-Akt and calcium signaling pathway. The results in vitro experiments showed that TWHF can dose-dependently reduce the release of β-hex and histamine induced by IgE, based on cell morphology, intracellular Ca²⁺ concentration, cell apoptosis rate and TNF-α release, TWHF was found to significantly inhibit RBL-2H3 cell degranulation, and TWPT was more effective than TPL in treating type I allergy. Results in vivo indicated that TWHF can dose-dependently inhibit plasma dye exudation and tissue edema in ears, backs and paws in PCA and PSA models. In addition, we also discovered that TWHF could regulate Th1/Th2 balance in PSA model in vivo. In conclusion, TWHF has the potential to be utilized as a medication to treat type I allergy. This work provides new perspectives on the pharmacological mechanism of TWHF.

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Alpha-onocerin is a triterpenoid derived from Huperzia phlegmaria which is used in ethnomedicine for the treatment of fever, headaches, pains and malaria. This study was conducted to evaluate the safety, antipyretic and anti-plasmodial activity of alpha-onocerin and artesunate (ART) co-administration in ICR mice for use in traditional medicine.

The anti-plasmodial effects of alpha-onocerin (10, 30, 100, 300 mg/kg) and ART (1, 2, 4, 8, 16 mg/kg) were assessed in P. berghei-infected mice. Alpha-onocerin /ART were administered with a fixed dose combination of their median effective doses (ED_50s) to determine the experimental ED₅₀ (Z_exp). An isobologram was developed to identify the nature of the interaction by comparing Z_exp with the theoretical ED₅₀ (Z_add).

Alpha-onocerin (300 mg/kg) showed a similar chemosuppression (93.51 ± 2.15%) to ART (2 mg/kg, i.p.) of 97.02 ± 0.27% in the 4-day suppressive test as well as in the prophylactic test with chemosuppression at 54.94% and 69.76% for alpha-onocerin (300 mg/kg) and artesunate (2 mg/kg, i.p.) respectively. All doses of alpha-onocerin significantly (p < 0.05) reduced pyrexia in 1 h and 2 h after their administration in the baker’s yeast test. ED₅₀s for ART and alpha-onocerin were 1.33 ± 0.11 and 13.64 ± 0.22 mg/kg, respectively. The Z_add, Z_exp and interaction index for alpha-onocerin /ART co-administration were 7.49 ± 3.46, 1.61 ± 0.78 and 0.22 respectively. The Z_exp for alpha-onocerin /ART laid below the additive isobole indicating significant (p < 0.001) synergistic activity with ART.

Alpha-onocerin showed analgesic effects, antipyretic and synergistic anti-plasmodial effects in P. berghei-infected mice.

Loranthus parasiticus Merr. (L. parasiticus) is a semiparasitic plant and it has antidiabetic effects. But potential application of L. parasiticus to improve insulin sensitivity in mice with type 2 diabetes remains unexplored.

Herein, we aimed to investigate the potential antidiabetic effects of L. parasiticus extract (LPE) on hyperglycemia and insulin sensitivity in C57BL/Ksj-db/db mice. C57BL/Ksj-db/db mice were divided into three groups: diabetic control, rosiglitazone, and LPE. Db/db-control group was fed a standard semi-synthetic diet (AIN-93 G), db/db-RG group was fed AIN-93 G supplemented with rosiglitazone (RG) (0.005%, w/w), and db/db-LPE group was fed AIN-93 G supplemented with LPE (0.5%, w/w) for 6 weeks. Mice supplemented with LPE exhibited significantly lower blood glucose and glycosylated hemoglobin levels than diabetic control mice. Compared with diabetic control mice, LPE-supplemented mice exhibited a significant reduction in the homeostatic index of insulin resistance. LPE supplementation stimulated the pIRS ^Tyr612 and Akt^Ser473, as well as the activation of PI3K in the skeletal muscle insulin signaling pathway. Furthermore, LPE supplementation significantly increased the pAMPK^Thr172 and ACC^Ser79 and the expression of plasma membrane GLUT4. LPE supplementation improves insulin sensitivity and alleviates hyperglycemia in diabetic mice.

Psoriasis is an incurable skin disease with a prevalence of 2–5% worldwide. The main lesions of psoriasis are epidermal hyper-proliferation, skin barrier damage, and excessive inflammatory response. As existing treatments clearly have a lot of limitations to psoriasis patient cure, so it is needed for solutions through natural product-based alternative research. Ellagic acid, a yellow-colored plant-derived polyphenol compound existed much in punica granatum L., is known to have anti-inflammatory and whitening activity but rarely been reported on psoriasis. So, we aimed to study the psoriasis control and mechanism of action at the molecular and cellular level by ellagic acid. First, the cytotoxic concentration was measured using the CCK-8 assay. As a result, no cytotoxicity was observed up to 20 μg/mL concentration, so it was applied to all subsequent experiments. Ellagic acid suppressed the mRNA expression of antimicrobial peptides (AMPs) such as β-defensin2, which are characteristically overexpressed in psoriasis lesions. In addition, it downregulated the mRNA expression level of inflammatory cytokines and chemokines such as CXC motif chemokine ligand 8 (CXCL8) and CC motif chemokine ligand 20 (CCL20). Moreover, we observed that ellagic acid significantly inhibited IκB-phosphorylation in signal pathway through Western blot. Lastly, the trans-epithelial electrical resistance (TEER) assay results also confirmed the skin barrier recovery effect due to the anti-inflammatory activity of ellagic acid. These results suggest ellagic acid has a very high possibility of being developed as a raw material could be applied to patients with sensitive skin or intractable skin diseases like psoriasis.

Cucurbita ficifolia’s fruit aqueous extract has been attributed with antidiabetic and anti-inflammatory properties, offering a promising alternative in addressing meta-inflammation. Meta-inflammation plays a pivotal role in the development of metabolic dysfunction, contributes to conditions such as obesity, diabetes mellitus, and metabolic syndrome. The interactions between adipocytes and macrophages within adipose tissue cause the onset of meta-inflammation, leading to disruptions in the secretomes and transcriptomes of inflammatory cytokines among other factors. We evaluated the effects of the aqueous extract from the fruit of Cucurbita ficifolia on the secretomes and transcriptomes of 3T3-L1 adipocytes and RAW-264.7 macrophages, by exchange of their conditioned mediums and in co-culture conditions. Adipocytes incubated with conditionate medium from macrophages treated with the extract exhibited an increase in GLUT-4 expression, and the protein release of TNFα, accompanied by a reduction in IL-1β. In contrast, macrophages incubated with conditionate medium from adipocytes treated with the extract exhibited inhibition the release of TNFα, IL-6, and IL-10, with TLR-4 expression reduction. Interestingly, under the conditions of indirect simultaneous co-culture, the release of TNFα, IL-6, and IL-1β was disrupted, increasing PPARγ expression in 3T3-L1 adipocytes. The salicin, compound reported in Cucurbita ficifolia extract, had a similar effect in this last model. The aqueous extract of Cucurbita ficifolia demonstrates the ability to suppress meta-inflammation by correcting the secretion patterns of TNFα and IL-6 in co-culture conditions. It effectively modulates the interactions between 3T3-L1 adipocytes and RAW-264.7 macrophages, leading to an improvement in the inflammatory cytokines profile.

Liver damage is one of the leading diseases, resulting in high morbidity. It is more relevant in the context of bad food habits, environmental pollution, and biohazards. The present study aimed to investigate the role of semi-purified water extract of Pueraria tuberosa on carbon tetrachloride (CCl4)-induced liver injury and also its mechanism of action regarding transcriptomic status in liver tissue about inflammation, hypoxia, and apoptosis. Liver injury was induced in Charles foster rats via intraperitoneal injection (IP) of CCl4, 0.1 mg/100gm body weight, diluted with olive oil (30%) twice a week for 20 days. PTWE was given via oral route daily simultaneously with CCl4 at the dose of 50 mg/100 g and 100 mg/100 g body weight. On 21st day all rats were sacrificed. Biochemical tests and histological studies were done. mRNA expression of bcl-2, caspase-3, bax, and GAPDH and protein expression of iNOS, BCL-2, HIF-1α, VEGF, β-Tubulin was done. Simultaneous treatment of PTWE with CCl4 decreased the level of NO, PC, SGOT, SGPT, ALP, LPO, and iNOS, HIF-1α, VEGF, bax, and caspase-3 expression. In addition, PTWE increased the SOD, Catalase, GSH level, and bcl-2 expression as well as normalized the architecture of hepatic tissue. Immunohistochemical staining showed the decreased accumulation of CD45, VEGF, α-SMA, collagen, and desmin after PTWE treatment. This study suggests that PTWE inhibits fibrosis by reducing the accumulation of α-SMA, collagen, and desmin in CCl4-induced toxicity. The mechanism of protective action is through its anti-inflammatory (iNOS, NO, CD45), anti-apoptotic (bcl-2, bax, caspase-3), anti-hypoxic (HIF-1α, VEGF), and anti-fibrotic (α-SMA, collagen, desmin) potentials.

Breast cancer is a prevalent and life-threatening disease affecting women globally. Despite advances in cancer treatment, there is a pressing need for effective and low-toxicity anticancer agents. Recent research has highlighted the potential of nanosized extracellular vesicles derived from edible plants in modulating cell function and facilitating biomolecule transport between cells. Mounting evidences suggests the anticancer potential of nanovesicles derived various edible plants against different types of cancer. However, the potential of nanovesicles derived from ginger in treating breast cancer remains unexplored.

In this study, we aimed to investigate the therapeutic effects of ginger derived nanovesicles (GiDNVs) on breast cancer cell lines (MDA-MB-231 and MDA-MB-468). To accomplish our goal, we isolated nanovesicles from ginger using the differential centrifugation method and characterized their size and integrity by employing DLS and FESEM. Subsequently, we evaluated the therapeutic effects of these GiDNVs on breast cancer cells. Our results demonstrated that GiDNVs inhibited cancer cell proliferation in a dosage and time-dependent way. Furthermore, flow cytometry analyses and DAPI staining demonstrated that the anti-proliferative effect of GiDNVs was attributed to the induction of apoptosis in cancer cells. Additionally, western blotting analysis showed that the apoptotic effect of GiDNVs on breast cancer cell was mainly mediated modulation by bcl-2, bax and caspase-3. This study contributes to the development of novel and effective anticancer agents with minimal toxicity. In nutstell these findings highlight the ability of GiDNVs as a novel and effective anti-cancerous agent for breast cancer treatment.

The plant Annona glabra L. (Annonaceae) has a history of traditional use in treating various ailments such as inflammation, joint pain, and arthritis. Despite this, there has been limited pharmacological research on its effectiveness for rheumatoid arthritis. This study explores the anti-arthritic properties and phytochemical composition of an aqueous-ethanolic extract (50:50) prepared from Annona glabra leaves. The study assessed the anti-arthritic potential through in vivo testing with Complete Freund Adjuvant models at doses of 100 and 200 mg/kg. Additionally, both qualitative and quantitative phytochemical analysis were conducted to identify the various compounds present in the extract. The findings demonstrated a dose-dependent anti-arthritic response in the Complete Freund Adjuvant model, displaying enhanced protection against arthritic lesions and body weight changes. Furthermore, Annona glabra exhibited significant improvements in altered hematological parameters, rheumatoid factor, and mitigated radiographic and histopathological alterations. The quantitative phytochemical analysis identified phenolic compounds and flavonoids in the extract. These results support the traditional efficacy of Annona glabra as a promising anti-arthritic agent, potentially suitable for inclusion in herbal formulations for the treatment of rheumatoid arthritis.

The in vitro antiadipogenic properties of oleoresin obtained from Nigella sativa L.(black cumin) seeds was evaluated in this study using 3T3-L1 cells as model cell line. Despite containing beneficial compounds like polyphenols, thymoquinone, flavonoids, and unsaturated fatty acids known for their antioxidant properties, its role in obesity management is not fully understood. We hypothesized that black cumin seed oleoresin treatment would inhibit differentiation of 3T3-L1 preadipocytes by regulating expression of transcription factors, peroxisome proliferator-activated receptor γ (PPAR-γ) and CCAAT enhancer binding protein α (C/EBP-α). Cells were cultured and differentiated for 8 days in Dulbecco modified Eagle media (DMEM) containing 10% fetal bovine serum, both in the absence (control) and presence of 25, 50 and 100 µg/ml oleoresin. Oil red O staining after differentiation revealed a dose-dependent, substantial reduction in lipid droplet accumulation in the differentiated adipocytes treated with oleoresin than differentiated control (DC) group. Molecular analysis revealed downregulation in cellular induction of PPAR-γ, C/EBP-α and sterol regulatory element-binding protein 1 (SREBP1) transcription factors. Furthermore, mRNA expression of particular target genes of these transcription factors— adiponectin, adipocyte fatty acid binding protein (aP2), leptin and fatty acid synthase (FAS) was also dose dependently inhibited in differentiated adipocytes by oleoresin treatment. The activation of adenosine monophosphate protein kinase (AMPK) and phosphorylation of its substrate acetyl-CoA carboxylase (ACC) was detected by western blotting showing a significant increase in their phosphorylated protein levels. Collectively, these findings suggest that black cumin seed oleoresin showed anti-obesity effects by inhibiting lipid droplet formation and modulating molecular pathways involved in adipogenesis, highlighting its potential as a natural therapeutic agent for obesity and related metabolic disorders.

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At present, there are no alternatives for doxorubicin (Dox), which is associated with cardiotoxicity. Countering the negative effects of Dox with natural compounds is gaining interest among the scientific community. Prior studies demonstrated that p-Coumaric acid (pCA) decreased the toxicity caused by Dox in cardiomyocytes and is expected to work through multiple cellular mechanisms. This study aimed to clarify the fundamental mechanism of how pCA protects the heart. Cardiomyocyte cells (H9c2) were treated with Dox, pCA, and a combination of pCA and Dox. After 24 h of treatment, gene expression of COX 2, NF-κß, PGC1-α, cytb, and TFAM was measured. Swiss ADME analysis was conducted to assess the drug-likeness characteristics, Pro-Tox for toxicity properties of pCA, and in silico analysis was performed to evaluate the interaction of pCA with Keap 1 protein. The mRNA expressions of COX-2 and NF-κß (p65) were found to be upregulated in Dox-treated cells among the different treatment groups whereas, the activity was found to be greatly reduced in pCA groups before and during Dox treatment. mRNA levels of PGC1-α, TFAM, and Cyt b were found to be upregulated in the pCA pre and cotreated groups when compared to Dox-treated cells indicating the involvement of mitochondrial biogenesis. In silico analysis showed that pCA has druggable properties with no toxicity, while it interacted with keap 1 protein. The results demonstrate that Dox treatment may aggravate myocardial injury which is alleviated by pCA by modulating the PGC1α and keap1 pathways thereby boosting mitochondrial biogenesis.