Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan最新文献

Objective: To investigate the effects of gut microbes regulation of the trimethylamine (TMA)/flavin containing monooxygenase 3 (FMO3)/trimethylamine N-oxide (TMAO) pathway on platelet aggregation in acute coronary syndrome (ACS) rats and the intervention of Huayu Qutan formula.

Methods: The ACS rats with syndrome of phlegm and blood stasis rats were established. Platelet, platelet aggregation, platelet activation markers and TMA/FMO3/ TMAO pathway were detected. Metagenomics technology was employed to analyze the characteristics of the gut microbiota.

Results: Huayu Qutan formula and gut microbes could inhibit high platelet reactivity and regulate the TMA/ FMO3/TMAO pathway. The dominant bacteria in ACS rats including but not limited to the major phyla, Firmicutes, Bacteroidetes, Actinobacteria, and Proteobacteria, also including some low abundance phyla, Fusobacteria, Verrucomicrobia, Spirochaetes, and Deferribacteres. The dominant bacteria in the Huayu Qutan formula group were Synergistetes, Deferribacteres, Deferribacteraceae, Faecalibacterium and Mucispirillum. In the Huayu Qutan formula combined with fecal bacteria enema group, the dominant bacteria were Verrucomicrobia, Verrucomicrobiae, Akkermansia and Verrucomicrobium. These gut microbiota were correlated with pathways such as Riboflavin metabolism and Arachidonic acid metabolism.

Conclusion: Huayu Qutan formula may prevent ACS by modulating gut microbes Synergistetes, Faecalibacterium and Allobaculum, regulating the iron metabolism of Deferribacteres, and driving the TMA/FMO3/TMAO pathway to regulate gut microbiota function, and improving platelet aggregation. Akkermansia may serve as a promising probiotic, which could drive TMA/FMO3/ TMAO pathway to regulate Arachidonic acid metabolism to improve platelet aggregation. The findings of this study provide a theoretical basis for the theory of "the heart is connected with the small intestine".

Objective: To explore the therapeutic potential of the Dujieqing (DJQ) decoction for multiple myeloma (MM) and elucidate its mechanism of action.

Methods: RPMI8226 cells were treated with DJQ-containing serum (DJQ-CS) and a Wnt/β-catenin pathway inhibitor, XAV-939. Cell counting kit-8 assay was used to examine cell viability, and flow cytometry was performed to examine apoptosis. Real-time polymerase chain reaction and Western blotting were used to evaluate the Wnt/β-catenin pathway family members in the cells. Subsequently, the RPMI8226 cells were subcutaneously injected into the left flank of none obesity disease and server combined immune-deficiency mice to replicate the xenograft tumor mouse models, which were treated with the DJQ decoction for 14 d. Hematoxylin and eosin staining was used to examine the pathological changes of the liver and kidney tissues, and to detect xenograft tumors. Wnt/β-catenin pathway family members were evaluated via Western blotting.

Results: DJQ-CS significantly reduced the mRNA and protein expression levels of β-catenin, c-myc, cyclin D1, and lymphoid enhancer binding factor 1 (LEF1) while inhibiting the proliferation of RPMI8226 cells and inducing their apoptosis. Similar results were observed when the Wnt/β-catenin pathway was suppressed by inhibitors. Moreover, in the mouse model of xenograft tumors, DJQ decoction not only reduced the tumor volume but also inhibited the protein levels of β-catenin, c-myc, cyclin D1, and LEF1. The histopathology of the mice also showed increased apoptosis in tumor tissues, while the DJQ decoction treatment did not cause any pathological damage to the kidneys or liver.

Conclusion: Our results indicate that the DJQ decoction suppresses tumor progression by inhibiting the Wnt/β-catenin pathway, offering a promising treatment approach for MM.

Objective: To explore the mechanism of Danggui Buxue decoction (, DBD) for the treatment of gastric ulcer (GU), based on network pharmacology and in vivo experiments.

Methods: A network pharmacology strategy was used to predict the main components, candidate targets, and potential signaling pathways. Then, molecular docking was performed to further investigate the interactions and binding affinities between the main components and primary targets. Finally, a mouse model of ethanol-induced gastric ulcers was established to confirm the efficacy and potential therapeutic benefits of DBD, and candidate targets were finally identified.

Results: A total of 22 active components and 220 target genes were found to be associated with DBD. In addition, 343 GU-related target genes and 57 target genes specific to DBD treatment of GU were identified. The Gene Ontology functional enrichment analysis revealed 510 entries for biological processes, 36 entries for cell composition, and 69 entries for molecular functions. In the pathway enrichment analysis, 143 signaling pathways were identified. Additionally, the molecular docking results revealed that the main active components of DBD exhibited a strong binding capacity with key proteins, including tumor necrosis factor, AKT serine/threonine kinase 1, interleukin-6, vascular endothelial growth factor, and interleukin-1 Beta. Among these, quercetin, kaempferol, formononetin, isorhamnetin, and beta-sitosterol displayed the strongest binding affinities for these key proteins. in vivo experiments showed that DBD pretreatment effectively protected gastric mucosa, and the benefits might be attributed to the downregulation of above key proteins.

Conclusions: Based on network pharmacology analysis and in vivo experiments, we conclude that DBD leads to the protection and healing of the gastric mucosa by targeting genes and pathways, thus effectively countering the development and progression of GU.

Objective: To evaluate the effect of Yiqi Liangxue Shengji prescription (, YQLXSJ) on cardiac function and outcomes in acute myocardial infarction (AMI) patients with myocardial ischemia-reperfusion injury (MIRI) and to determine its clinical efficacy.

Methods: This prospective, randomized, double-blind, placebo-controlled trial enrolled hospitalized patients with AMI who underwent percutaneous coronary intervention and experienced MIRI either intraoperatively or postoperatively. Participants were randomly allocated to the treatment group, which received YQLXSJ, or the control group, which received a placebo, concurrent with standard Western Medicine therapy. The intervention period lasted 8 weeks. The primary outcome measure was left ventricular ejection fraction (LVEF), determined by echocardiography. Secondary outcomes included N-terminal pro brain natriuretic peptide (NT-proBNP) and cardiac troponin I (cTnI) levels, left ventricular internal diameter, major adverse cardiovascular events (MACE), angina pectoris scores, and Chinese medicine evidence scores.

Results: Following 8 weeks of intervention, the treatment group demonstrated a significant increase in LVEF and a marked reduction in NT-proBNP when compared to the control group. There was also a significant decrease in peak cTnI levels, Chinese medicine evidence scores, and angina pectoris scores. The control group's left ventricular end-systolic diameter (LVESD) significantly increased compared to baseline after 8 weeks (P < 0.05), whereas the treatment group's LVESD showed no significant change from baseline (P > 0.05). Although the treatment group showed a downward trend in MACE incidence compared to the control group, this difference was not statistically significant (P > 0.05).

Conclusions: This study demonstrated that the addition of YQLXSJ to standard therapy can improve cardiac function and alleviate clinical symptoms in AMI patients with MIRI, and also showed a potential to mitigate the incidence of MACE. Furthermore, YQLXSJ displayed a favorable safety profile in clinical application.

Objective: To investigate the effects of Jiawei Huangqi Guizhi decoction on chronic atrophic gastritis (CAG) in rats and its modulation of the phosphatidylinositol 3-kinase/protein kinase B/ mechanistic target of rapamycin complex 2 (PI3K/Akt/ mTORC2) signaling pathway.

Methods: CAG was induced in rats and treated with high-, medium-, or low-dose Jiawei Huangqi Guizhi decoction. Gastric histopathology was observed by hematoxylin and eosin staining. Serum levels of gastrin, PI3K, Akt, and mTORC2 were detected by enzyme-linked immunosorbent assay. Gene and protein expression levels were analyzed by reverse transcription polymerase chain reaction and western blot.

Results: The decoction alleviated gastric mucosal injury, reduced inflammation, and restored epithelial structure. It regulated PI3K, Akt, and mTORC2 expression at both mRNA and protein levels.

Conclusion: Jiawei Huangqi Guizhi decoction may prevent CAG progression by improving gastric tissue and modulating the PI3K/Akt/mTORC2 signaling pathway.

Microglia (MG) are immune effector cells in the central nervous system (CNS) and play a pivotal role in the pathogenesis of various CNS diseases. Alzheimer's disease (AD) is defined as a severe chronic degenerative neurological disease in humans. The amyloid cascade hypothesis is a hypothesis on the pathogenesis of AD that suggests that abnormal extracellular aggregation of β-amyloid (Aβ) peptides is the main cause of the disease. Although this hypothesis has been found to be convincing, a growing body of evidence suggests that it does not fully explain the pathogenesis of AD. Neuroinflammation is a crucial element in the pathogenesis of AD, as evidenced by elevated levels of inflammatory markers and the identification of AD risk genes associated with innate immune function. This paper will first summarize the impact of microglia-mediated neuroinflammation on AD, exploring the phenotypic changes that follow microglia activation. Secondly, the interactions between microglia, Aβ, microtubule-associated protein, apolipoprotein E and neurons are thoroughly investigated, with particular focus on the interactive mechanisms. Furthermore, the recent progress and prospects of microglia as a diagnostic and therapeutic target for AD are analysed. A review of the literature on the mechanisms regulating MG for AD at home and abroad revealed that acupuncture modulation of microglia could help to delay the progression of AD. This was followed by an extensive discussion of the clinical possibilities and scientific validity of acupuncture treatment for AD, with the aim of providing new insights for acupuncture modulation of MG targeting for the treatment of AD.

Objective: To evaluate the efficacy of electroacupuncture (EA) at scalp motor area for treating post-stroke wrist dyskinesia and its influence on the function of wrist movement-related agonistic muscles.

Methods: A randomized, single-blind, controlled clinical trial was conducted. Sixty-six patients undergoing post-stroke wrist dyskinesia were enrolled and randomized 1 : 1 to EA or control group. Patients in the control group received manual acupuncture in the scalp motor area (MS 6) on the lesion side. The same acupoint was selected to accept EA stimulation in the EA group. All patients were treated six times a week for three weeks. The primary outcome was the Chinese Stroke Scale (CSS) score. The secondary outcomes included upper limb-related Barthel Index (BI) score, active range of motion (AROM) of the wrist joint, and root mean square (RMS) of the four agonistic muscles associated with wrist motion on the hemiplegic side of patients, i. e., the extensor carpi radialis longus (ECRL), extensor digitorum (ED), flexor carpi radialis (FCR) and flexor carpi ulnaris (FCU). The above indicators were measured before and after three weeks of treatment.

Results: After 3-week treatment, the CSS score and AROM of wrist dorsiflexion of the EA group were better than those in the control group (P = 0.038, P = 0.047). The differences between the two groups of BI scores and AROM of wrist flexion were not significant (P > 0.05). All RMS of the EA group were higher than those in the control group (ECRL: P = 0.047, ED: P = 0.048, FCR: P = 0.049, FCU: P = 0.047). The total effective rate in the EA group was 87.50% (28/32), which was higher than that in the control group (77.42%, 24/31, P = 0.048).

Conclusion: EA stimulation of the scalp motor area can promote the recovery of the strength and function of the agonistic muscles related to wrist movement and effectively improve post-stroke wrist dyskinesia.

Objective: To investigate the mechanism of electroacupuncture of sympathetic nerve activity and blood pressure reduction in the hypothalamic paraventricular nucleus (PVN) of spontaneous hypertensive rats (SHRs).

Methods: A total of 64 male SHRs were divided into four groups: model, sham-operated (Sham), electro-acupuncture (EA), and N-methyl-D-aspartate receptor antagonist and electroacupuncture (NRA + EA). In addition, 16 Wistar-Kyoto rats were used as controls. PVN stereotaxic surgery was performed in both the Sham and NRA + EA groups, while the EA and NRA + EA groups received 14 d of electroacupuncture. Blood pressure (BP) and heart rate (HR) were measured the day before the intervention and every other day. After 14 d of intervention, the rats in each group were tested for renal sympathetic nerve activity (RSNA). The associated factor levels were determined using Western blotting, reverse transcription-polymerase chain reaction (RT-PCR), enzyme-linked immunosorbent assay (ELISA) and immunofluorescence assays.

Results: In comparison to the model group, the EA and NRA + EA groups had significantly lower BP, HR, and RSNA (P < 0.01). The expression of N-methyl-D-aspartate receptor (NMDAR), angiotensin II (Ang II), angiotensin II type 1 (AT1), tumor necrosis factor-α, interleukin-1β, norepinephrine and arginine vasopressin was significantly lower in the EA and NRA + EA groups (P < 0.01). Moreover, the antihypertensive effect of NRA+EA group outperformed to the EA group.

Conclusions: Electroacupuncture effectively reduced the BP and sympathetic nerve excitability in SHRs. The mechanism was linked to the inhibition of NMDAR-mediated Ang II /AT1 and the inflammatory response in PVN.

Objective: To clarify the effect of Hamayou (Oviductus Ranae) protein hydrolysate (ORPH) on depression and its exact underlying mechanism from a new perspective.

Methods: We used the Chronic Unpredictable Mild Stress (CUMS) method to prepare a mouse model of depression and lipopolysaccharide (LPS) to prepare a model of BV2 cellular inflammation to investigate the antidepressant effect and mechanism of action of ORPH. Behavioral changes in mice and cerebral blood flow were detected by behavioral experiments and scatter imaging. Levels of corticosterone (CORT), proinflammatory cytokines and neurotransmitter were detected by enzyme-linked immunosorbent assay. Furthermore, hematoxylin-eosin staining, Tunel staining were used to evaluate the effect of ORPH. The distribution and expression of ionized calcium bindingadaptor molecule-1 (Iba-1) in mouse hippocampal tissue and BV2 cells were detected by immunofluorescence. Mitogen-activated protein kinase (MAPK) pathway related protein expression was detected by Western blot.

Results: ORPH improved depression-like behavior, ameliorated brain tissue damage and apoptosis, and inhibited microglia activation in brain tissue in mice. In addition, ORPH reduced expression of B-cell lymphoma-2 (Bcl-2)-associated X (Bax), cysteinyl aspartate specific proteinase 3 (Caspase3), cysteinyl aspartate specific proteinase 9 (Caspase9), nuclear factor- kappa B (NF-κB), phosphorylation-p38 (p-p38), phosphorylation-Jun N-terminal kinase (p-JNK) proteins, and increased expression of Bcl-2, inhibitory kappa B alpha (IκB-α), phosphorylation-extracellular regulated protein kinases 1/2 (p-ERK1/2) proteins. On the other hand, there were fewer Iba-1-positive cells, lower expression of NF-κB, p-p38, p-JNK and p-ERK1/2 proteins, and higher expression of IκB-α proteins in BV2 cells in the ORPH group. In addition, ORPH increased 5-hydroxytryptamine, norepinephrine levels and decreased CORT, interleukin-1β (IL-1β), interleukin -6 (IL-6), tumor necrosis factor-α (TNF-α) levels.

Conclusion: ORPH was able to improve depression-like behaviors and that it took effects by promoting cerebral blood flow, inhibition of hypothalamic-pituitary-adrenal axis overactivation, improving the structural damage of hippocampal tissues, and inhibiting the inflammatory response. ORPH can reduced neuronal damage and inhibiting apoptosis by promoting the MAPK pathway.