To scrutinize the consequences and relevant mechanisms of electroacupuncture (EA) on irritable bowel syndrome (IBS).
Randomly assigned to normal, model, and EA groups were male C57BL/6 mice. Water avoidance stress (WAS) was employed to establish experimental irritable bowel syndrome (IBS) mouse models. Seven days of EA treatment, administered bilaterally to Tianshu (ST 25) and Zusanli (ST 36) acupoints, were given to mice in the EA group, each treatment lasting 15 minutes. Mice abdominal withdrawal reflex (AWR) tests and intestinal motility tests served to ascertain visceral sensitivity and intestinal motility. Immunofluorescence, real-time polymerase chain reactions (PCR), and Western blot analyses were employed to quantify the expression levels of tight junction proteins (TJPs) and inflammatory cytokines within colon tissues.
The effects of EA on visceral hypersensitivity and intestinal hypermotility were notable in WAS-induced IBS mice. Subsequently, EA prompted an increase in the expression of zonula occludens (ZO)-1, claudin-1, and occludin, along with a reduction in interleukin (IL)-8, interferon (IFN)-γ, and tumor necrosis factor (TNF)-α production in water avoidance stress (WAS)-induced irritable bowel syndrome (IBS) mice.
EA ameliorated the effects of WAS-induced IBS in mice, accomplishing this by upholding intestinal barrier functions and inhibiting inflammatory cytokine expression.
EA countered WAS-induced IBS in mice through improvements in intestinal barrier functions and the reduction of inflammatory cytokine expression.
To research the possible mechanisms of action through which the combined treatment of Tongdu Tiaoshen acupuncture and Xiaoxuming decoction (XXMD) might alleviate Parkinson's disease (PD).
A total of 96 C57BL/6 mice were randomly assigned to eight groups of 12 mice each: a blank control group, a model group, a medication group, an acupuncture group, a high-dose XXMD group (XXMD-H), a low-dose XXMD group (XXMD-L), an acupuncture plus high-dose XXMD group (A+H), and an acupuncture plus low-dose XXMD group (A+L). Six weeks after treatment, an examination revealed dopamine (DA) neurons and the pathological changes within the tyrosine hydroxylase (TH) positive cellular structures. To quantify the levels of dopamine (DA) and interleukins (IL-1, IL-6, IL-10), along with tumor necrosis factor alpha (TNF-), an enzyme-linked immunosorbent assay (ELISA) was employed. The substantia nigra was further analyzed to detect the mRNA levels of PINK1 and Parkin, and the protein expression of Nix, PINK1, and Parkin.
The dual-treatment strategy proved effective in alleviating the symptoms characteristic of Parkinson's disease. genetic swamping The combined treatment regimen led to a substantial upregulation of Nix, Parkin, and PINK1 protein expression, and an elevated mRNA level of PINK1 and Parkin in the substantia nigra as compared to the model group, yielding statistically significant findings (<0.00001, <0.0001, <0.001, or <0.005). Combined treatment clearly lowered pro-inflammatory cytokine levels, while IL-10 levels increased substantially, reaching statistical significance (<0.001).
Combined treatment demonstrated superior efficacy in ameliorating the pathological damage to dopamine neurons in PD mice compared to individual therapies. The mechanism could be due to up-regulated mitochondrial autophagy levels and improved mitochondrial function. These results provide fresh avenues for examining the interplay of Tongdu Tiaoshen acupuncture and XXMD therapies for treating Parkinson's Disease.
A synergistic effect was evident when comparing the efficacy of the combination therapy to individual treatments, leading to more effective reduction of pathological damage to dopamine neurons in PD mice. NSC 27223 concentration The mechanism's likely explanation is the up-regulation of mitochondrial autophagy and a consequent enhancement of mitochondrial function. These results detail a novel perspective on the co-treatment mechanism of Tongdu Tiaoshen acupuncture and XXMD in managing PD.
Analyzing the combinatorial and molecular effects of Zuogui (ZGP) and Yougui pills (YGP) in alleviating 4-vinyl cyclohexene diepoxide (4-VCD)-induced perimenopausal syndrome (PMS) forms the basis of this study.
Treatment with ZGP, YGP, ZGP + YGP, estradiol valerate (EV), and Gengnian An (GNA) in the 4-VCD-induced PMS mouse model was followed by assessment of uterine and ovarian indices and serum sex steroid hormone levels. The potential pharmacological effects and molecular mechanisms of ZYP and YGP were examined using a combination of histopathological examinations, ingredient-target network predictions, Western blotting, and real-time quantitative polymerase chain reaction (RT-qPCR) analyses.
ZGP and YGP treatment demonstrably improves estrous cyclicity and prevents uterine pathology. After the administration of ZGP and YGP, a return to normal levels was observed for sex hormones such as AMH, E2, FSH, LH, P, and T. Ingredient-target network analysis determined that the five ingredients shared by ZGP and YGP formulations directly impact 53 targets that also participate in the PMS pathway. A further pathway enrichment analysis suggested that ZGY and YGP are likely to control apoptosis and other critical pathways associated with PMS. In-vivo investigations on the effect of ZGP and YGP on PMS indicated a suppression of apoptosis, achieved through a reduction in caspase-3 and BAX protein levels and an increase in the ratio of BCL2 to BAX and BCL2 levels. cutaneous autoimmunity Significantly, the modulation achieved through ZGP and YGP treatment surpassed the effects seen with either ZGP or YGP treatment alone.
Novel anti-PMS agents, ZGP and YGP, function by restoring hormonal balance, safeguarding the uterine lining, and modulating apoptosis.
The novel anti-PMS agents, ZGP and YGP, achieve their results through the restoration of altered hormonal profiles, the preservation of the uterine integrity, and the regulation of apoptotic cell death.
To assess the anti-tumor efficacy and potential mechanisms of action of Sanwu Baisan Decoction (SWB) against colorectal cancer (CRC) in a mouse model.
An evaluation of the therapeutic effect was undertaken by considering body weight gain, tumor volume, the rate of tumor growth inhibition, histological alterations within tumor tissues, and apoptosis. Measurements of plasma interleukin 6 (IL-6), interleukin 17 (IL-17), and interferon (IFN-) levels served to investigate anti-tumor immunity. Morphological changes within the gut were evaluated through the application of histological staining techniques and the examination of tight junction protein expressions. A 16S rRNA gene sequencing method was utilized to ascertain the structure of the gut microbiota. The toll-like receptor 4 (TLR-4)/cyclooxygenase 2 (COX-2)/prostaglandin E2 (PGE-2) pathway's presence was scrutinized in both colon tissue and tumor specimens.
SWB demonstrated remarkable anti-tumor efficacy in mice with colorectal cancer, as evidenced by a decrease in tumor volume and an increase in the rate of tumor growth arrest. The anti-tumor action of SWB correlated with a rise in plasma levels of the anti-tumor immune cytokines IL-6, IL-17, and IFN-. Subsequent studies found that well-being (SWB) also upregulates the expression of occluding junctions and encourages the prevalence of beneficial gut microorganisms, , , and . Importantly, the results suggested that SWB's anti-tumor mechanisms might encompass the induction of cancer cell apoptosis and the inhibition of the TLR-4/COX-2/PGE-2 pathway in both colon tissue and tumor samples.
Mice bearing colorectal carcinoma treated with SWB displayed a strong reduction in tumor growth, potentially resulting from the stimulation of anti-cancer cytokine secretion, induction of cancer cell apoptosis, maintenance of a healthy gut microbiota, and inhibition of tumor development through disruption of the TLR-4/COX-2/PGE-2 signaling pathway.
SWB displays significant efficacy against colorectal carcinoma in mice, potentially achieved through enhancing the production of anti-tumor immune cytokines, facilitating cancer cell apoptosis, maintaining a healthy gut microbiome, and hindering tumor formation by disrupting the TLR-4/COX-2/PGE-2 pathway.
Salvianolic acid B (SalB)'s regulatory effect on trophoblast cells in preeclampsia (PE) is the focus of this investigation.
Following HO induction and treatment with varying concentrations of SalB, the viability of HTR-8/Svneo human extravillous trophoblast cells was determined via 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assays. The levels of superoxide dismutase, glutathione-Px, and malondialdehyde, indicators of oxidative stress, were measured using the corresponding 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. This study employed wound healing and Transwell assays to quantify cell invasion and migration. To ascertain the expression levels of epithelial-mesenchymal transition-related proteins, Western blot analysis was employed. Using reverse transcription-quantitative real-time polymerase chain reaction (RT-qPCR) and western blot analysis, researchers further investigated the mechanisms underlying SalB to determine the expression levels of matrix metallopeptidase 9 (MMP-9) and phosphatidylinositol-45-bisphosphate 3-kinase (PI3K)/protein kinase B (Akt).
SalB's impact on HTR-8/Svneo cells involved augmented activity and a reduction in HO-induced oxidative stress, ultimately leading to enhanced invasion and migration of trophoblast cells. Subsequently, the expression levels of MMP-9 and members of the PI3K/Akt signaling pathway were found to be significantly diminished. The pathway agonist, LY294002, and the MMP-9 inhibitor, GM6001, countered SalB's impact on HO-induced cells.
SalB facilitated the invasion and migration of HO-induced HTR-8/Svneo trophoblast cells, a process driven by elevated MMP-9 expression and activation of the PI3K/Akt signaling pathway.
By elevating MMP-9 and the PI3K/Akt signaling pathway, SalB encouraged the invasion and migration of HO-induced HTR-8/Svneo trophoblast cells.