To assess the influence and underlying processes of electroacupuncture (EA) on irritable bowel syndrome (IBS).
Randomly assigned to normal, model, and EA groups were male C57BL/6 mice. Mice exhibiting irritable bowel syndrome (IBS) were created by subjecting them to water avoidance stress. Mice of the experimental group (EA) underwent bilateral electro-acupuncture (EA) stimulation of Tianshu (ST 25) and Zusanli (ST 36) acupoints for seven days, with each treatment lasting 15 minutes. Intestinal motility and visceral sensitivity of mice were assessed by means of abdominal withdrawal reflex (AWR) tests and intestinal motility tests. Utilizing immunofluorescence, real-time PCR, and Western blotting, the expression levels of tight junction proteins (TJPs) and inflammatory cytokines in colon tissues were determined.
In WAS-induced IBS mice, EA effectively reduced both visceral hypersensitivity and intestinal hypermotility. EA, in particular, encouraged the elevation of zonula occludens (ZO)-1, claudin-1, and occludin levels, and conversely decreased the levels of interleukin (IL)-8, interferon (IFN)-γ, and tumor necrosis factor (TNF)-α in water avoidance stress (WAS)-induced irritable bowel syndrome (IBS) mice.
By bolstering intestinal barrier function and diminishing inflammatory cytokine expression, EA countered WAS-induced IBS in mice.
EA's impact on WAS-induced IBS in mice involved enhancing intestinal barrier function and reducing the levels of inflammatory cytokines.
A study to determine the underlying mechanisms of the combined therapeutic approach of Tongdu Tiaoshen acupuncture and Xiaoxuming decoction (XXMD) in Parkinson's disease (PD).
Eight groups (12 mice per group) of C57BL/6 mice were randomly assigned: a blank control, a model, a medication, an acupuncture, a high-dose XXMD (XXMD-H), a low-dose XXMD (XXMD-L), a combined acupuncture and high-dose XXMD (A+H), and a combined acupuncture and low-dose XXMD (A+L) group. Six weeks after treatment, an examination revealed dopamine (DA) neurons and the pathological changes within the tyrosine hydroxylase (TH) positive cellular structures. The enzyme-linked immunosorbent assay (ELISA) was the method of choice for determining the concentration of dopamine (DA) and the levels of interleukin-1 (IL-1), interleukin-6 (IL-6), interleukin-10 (IL-10), and tumor necrosis factor-alpha (TNF-). The substantia nigra was also examined for the mRNA levels of PINK1 and Parkin, and the protein expression of Nix, PINK1, and Parkin.
Symptomatic relief in Parkinson's disease patients was significantly enhanced by the combined treatment approach. click here The substantia nigra, under combined treatment, exhibited a notable increase in the protein expression of Nix, Parkin, and PINK1, along with the mRNA levels of PINK1 and Parkin, when compared to the model group, with statistically significant results (<0.00001, <0.0001, <0.001, or <0.005). Moreover, the levels of pro-inflammatory cytokines demonstrably decreased following combined therapy, while IL-10 levels exhibited a significant rise (<0.001).
When compared to the effects of individual treatments, combined therapy showed a more substantial improvement in the pathological damage to dopamine neurons in PD mice. The mechanism is potentially linked to heightened mitochondrial autophagy and strengthened mitochondrial function. Insights into the co-treatment of PD with Tongdu Tiaoshen acupuncture and XXMD are newly provided by these research results.
The combined therapeutic regimen was found to be significantly more effective in ameliorating the pathological damage to dopaminergic neurons in PD mice, when contrasted with the application of each treatment alone. severe bacterial infections The up-regulation of mitochondrial autophagy and enhanced mitochondrial function might explain the potential mechanism. Fresh insights into the co-treatment mechanism of Tongdu Tiaoshen acupuncture and XXMD for PD are provided by these results.
An investigation into the molecular mechanisms and combinatorial effects of Zuogui (ZGP) and Yougui pills (YGP) on 4-vinyl cyclohexene diepoxide (4-VCD)-induced perimenopausal syndrome (PMS).
In a 4-VCD-induced PMS mouse model, serum sex steroidal hormone levels, as well as uterine and ovary indices, were measured following treatment with ZGP, YGP, ZGP + YGP, estradiol valerate (EV), and Gengnian An (GNA). To determine the possible pharmacological effects and molecular mechanisms of ZYP and YGP, histopathological examinations, ingredient-target network predictions, Western blotting, and real-time quantitative polymerase chain reaction (RT-qPCR) analyses were conducted.
Treatment with ZGP and YGP is strikingly effective in restoring estrous cyclicity and preventing any pathological damage to the uterus. The administration of ZGP and YGP led to the re-establishment of normal levels of altered sex hormones, specifically AMH, E2, FSH, LH, P, and T. A network analysis of the ingredients and their corresponding targets indicated that five ingredients present in both the ZGP and YGP formulations are linked to 53 targets with overlapping roles in PMS. Further investigation using pathway enrichment analysis indicated that ZGY and YGP may play a role in the regulation of apoptosis and other essential pathways during PMS. Studies conducted in living organisms showcased that ZGP and YGP inhibited PMS-induced apoptosis by decreasing caspase-3 and BAX protein levels and increasing BCL2/BAX and BCL2 expression. microbiome modification Modulation effects were considerably enhanced, or at least enhanced to a noteworthy degree, when both ZGP and YGP treatments were used together, contrasting with the results achieved by ZGP or YGP treatment alone.
Restoring hormonal levels, protecting the uterine structure, and modulating apoptosis are the mechanisms of action for the novel anti-PMS agents, ZGP and YGP.
ZGP and YGP, novel anti-PMS agents, function by re-establishing the balance of hormones, preserving the integrity of the uterus, and controlling apoptotic activity.
To assess the anti-tumor efficacy and potential mechanisms of action of Sanwu Baisan Decoction (SWB) against colorectal cancer (CRC) in a mouse model.
The therapeutic effect was determined via observation of body weight gain, tumor volume, tumor growth inhibition percentage, along with histological alterations and apoptosis in the tumor tissue samples. Anti-tumor immunity was evaluated by quantifying the plasma concentrations of the anti-tumor cytokines interleukin 6 (IL-6), interleukin 17 (IL-17), and interferon (IFN-). An evaluation of gut morphological changes involved both histological staining and the analysis of tight junction protein expression. 16S rRNA gene sequencing served as the method for characterizing gut microbiota composition. Samples of colon tissue and tumor were examined to identify the classical toll-like receptor 4 (TLR-4)/cyclooxygenase 2 (COX-2)/prostaglandin E2 (PGE-2) pathway's role.
SWB displayed strong anti-tumor activity against colorectal cancer in mice, manifested through a decrease in tumor volume and an increase in the rate of tumor growth retardation. The anti-tumor effect of SWB was characterized by elevated plasma levels of the anti-tumor immune cytokines IL-6, IL-17, and IFN-. Additional research into the impact of subjective well-being (SWB) indicated that it augmented the expression of occluding proteins, and fostered a rise in the number of beneficial gut bacteria, , , and . Furthermore, the anti-tumor effects of SWB were indicated by its capacity to induce cancer cell apoptosis and inhibit the TLR-4/COX-2/PGE-2 pathway, both in colon tissue and tumor samples.
In a murine model of colorectal carcinoma, SWB demonstrated a substantial anti-tumor response, potentially stemming from the stimulation of anti-tumor immune cytokines, induction of cancer cell apoptosis, maintenance of the gut microbiota balance, and inhibition of tumorigenesis by interfering with the TLR-4/COX-2/PGE-2 pathway.
SWB's impressive anti-tumor performance in mice with colorectal carcinoma may be due to its capacity to promote the release of anti-tumor immune cytokines, induce apoptosis in cancer cells, maintain a healthy gut microbiome, and prevent tumorigenesis by inhibiting the TLR-4/COX-2/PGE-2 signaling cascade.
To explore the regulatory influence of salvianolic acid B (SalB) on trophoblast cells in the context of preeclampsia (PE).
3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assays were used to quantify the survival of human extravillous trophoblast HTR-8/Svneo cells exposed to HO and subsequently treated with various concentrations of SalB. Detection of superoxide dismutase, glutathione-Px, and malondialdehyde, markers of oxidative stress, was accomplished using the respective assay kits. To detect cell apoptosis, the Terminal deoxynucleotidyl transferase (TdT) dUTP Nick-End Labeling (TUNEL) approach was used. Western blot analysis further served to measure the expression of apoptosis-related proteins. The levels of cell invasion and migration were determined in the current study via wound healing and Transwell assays. For the purpose of detecting the expression levels of epithelial-mesenchymal transition-related proteins, Western blot analysis was carried out. To delve deeper into the SalB-related mechanisms, reverse transcription-quantitative real-time polymerase chain reaction (RT-qPCR) and western blot analysis were employed to quantify the expression of matrix metallopeptidase 9 (MMP-9) and phosphatidylinositol-45-bisphosphate 3-kinase (PI3K)/protein kinase B (Akt).
HO-induced alterations in trophoblast cells were counteracted by SalB, which spurred heightened activity in HTR-8/Svneo cells, alongside diminishing oxidative stress and prompting trophoblast cell invasion and migration. Moreover, the levels of MMP-9 and components of the PI3K/Akt signaling pathway were substantially reduced. LY294002, a pathway agonist, and GM6001, an MMP-9 inhibitor, reversed the detrimental effects of SalB on HO-induced cells.
The invasion and migration of HO-induced HTR-8/Svneo trophoblast cells were promoted by SalB's upregulation of MMP-9, coupled with the activation of the PI3K/Akt signaling pathway.
Upregulation of MMP-9 and the PI3K/Akt signaling pathway by SalB promoted the invasion and migration of HO-induced HTR-8/Svneo trophoblast cells.