Acupuncture-moxibustion therapy has been known to ameliorate the symptoms of functional gastrointestinal disorders (FGIDs), although its mechanism remains unclear. The paper reviews the articles on acupuncture-moxibustion therapy for FGIDs in recent 5 years, and it is revealed that acupuncture-moxibustion therapy can alleviate FGIDs symptoms through regulating gastrointestinal motility, modulating visceral hypersensitivity, improving the impaired gastric-duodenal mucosal barrier and inflammation, balancing intestinal microbiota, and adjusting the gut-brain axis. Currently, the molecular mechanism of acupuncture-moxibustion therapy remains unknown for FGIDs, the specific disease target is not identified, and the interaction among various molecules is not elucidated adequately. The researches in the future should employ advanced technologies and methodologies to comprehensively and deeply explore and clarify the mechanism of acupuncture- moxibustion therapy for FGIDs.
Humans ; Moxibustion ; Acupuncture Therapy ; Gastrointestinal Diseases/microbiology* ; Animals

Objective:To investigate the effects of Schisandrin A on the proliferation and apoptosis of prostate cancer cell and its mechanism.Methods:Human prostate cancer DU145 cell were cultured in vitro and grouped into DU145 group (normal culture), Schisandrin A L group (50 μmol/L Schisandrin A was added), Schisandrin A M group (100 μmol/L Schisandrin A was added), Schisandrin A H group (150 μmol/L Schisandrin A was added) and Simvastatin group (50 μmol/L Simvastatin was added). Cell morphology of each group was observed under microscope, cell proliferation ability was detected by CCK8 method, cell migration ability was detected by cell scratch assay, cell invasion ability was detected by Transwell assay, and cell apoptosis was detected by flow cytometry, the expression of phosphorylation (p) - mammalian STE20-like protein kinase 1 (MST1), MST1, p-large tumor suppressor 1 (LATS1), LATS1, p-Yes associated protein (YAP) and YAP protein were detected by Western blotting. Measurement data were expressed as mean± standard deviation ( ± s), one-way ANOVA for comparisons between multiple groups, and t-test for comparisons between two groups. Results:Compared with DU145 group, the number of cells in Schisandrin A L, M, H groups and Simvastatin group decreased, and the cells gradually shrunk and the spacing became larger, the cell survival rate [(100.00±0.00)%, (88.41±9.36)%, (62.34±7.31)%, (42.57±5.01)%, (45.47±5.65)%], migration [(90.11±13.43)%, (74.16±8.08)%, (57.53±7.34)%, (41.34±6.79)%, (43.44±5.26)%] and invasion [(89.01±10.31)%, (73.11±9.23)%, (55.62±7.67)%, (41.13±6.35)%, (40.36±5.68)%], and the expression of p-YAP/YAP protein (0.98±0.08, 0.83±0.11, 0.69±0.07, 0.55±0.07, 0.53±0.05) were significantly decreased, the apoptosis rate [(2.88±0.34)%, (5.20±0.57)%, (8.37±0.94)%, (12.71±1.58)%, (12.03±2.21)%] and the expression of p-MST1/MST1 (0.41±0.04, 0.53±0.07, 0.75±0.07, 0.89±0.08, 0.88±0.07] and p-LATS1/LATS1 protein (0.40±0.04, 0.52±0.06, 0.64±0.06, 0.77±0.08, 0.79±0.08) were significantly increased, and the differences were statistically significant ( P<0.05). Conclusion:Schisandrin A may inhibit the proliferation of prostate cancer cell and promote cell apoptosis by inhibiting Hippo-YAP signaling pathway.

Coronary restenosis is an important cause of poor long-term prognosis in patients with coronary heart disease. Here, we show that lysine methyltransferase SMYD2 expression in the nucleus is significantly elevated in serum- and PDGF-BB-induced vascular smooth muscle cells (VSMCs), and in tissues of carotid artery injury-induced neointimal hyperplasia. Smyd2 overexpression in VSMCs (Smyd2-vTg) facilitates, but treatment with its specific inhibitor LLY-507 or SMYD2 knockdown significantly inhibits VSMC phenotypic switching and carotid artery injury-induced neointima formation in mice. Transcriptome sequencing revealed that SMYD2 knockdown represses the expression of serum response factor (SRF) target genes and that SRF overexpression largely reverses the inhibitory effect of SMYD2 knockdown on VSMC proliferation. HDAC3 directly interacts with and deacetylates SRF, which enhances SRF transcriptional activity in VSMCs. Moreover, SMYD2 promotes HDAC3 expression via tri-methylation of H3K36 at its promoter. RGFP966, a specific inhibitor of HDAC3, not only counteracts the pro-proliferation effect of SMYD2 overexpression on VSMCs, but also inhibits carotid artery injury-induced neointima formation in mice. HDAC3 partially abolishes the inhibitory effect of SMYD2 knockdown on VSMC proliferation in a deacetylase activity-dependent manner. Our results reveal that the SMYD2-HDAC3-SRF axis constitutes a novel and critical epigenetic mechanism that regulates VSMC phenotypic switching and neointimal hyperplasia.

Three novel sesquiterpenoid heterodimers,designated as auckcostusolides A-C(1-3),were isolated from Aucklandia costus leaves.The structures of compounds 1-3 were elucidated through comprehensive spectroscopic analysis,with their absolute configurations established using a combination of X-ray single-crystal diffraction and electronic circular dichroism(ECD)calculations.Notably,compounds 1 and 2,despite sharing identical planar structures derived from two identical sesquiterpenoids,exhibited oppos-ite configurations at C-11 and C-8'.This configurational difference can be attributed to distinct Diels-Alder cycloaddition processes between the sesquiterpenoid monomers.Additionally,the cytotoxic effects of compounds 1-3 were evaluated against colorectal can-cer HCT116 cells,fibrosarcoma HT1080 cells,and hepatocellular carcinoma HepG2 cells.Compounds 1-3 induced cell death was characterized by endoplasmic reticulum(ER)swelling and cytoplasmic vacuolization,typical morphological changes associated with paraptosis.Mechanistic studies revealed that compounds 1 and 3 triggered paraptosis-like cell death through the accumulation of react-ive oxygen species(ROS),activation of ER stress,and stimulation of the MAPK signaling pathway.

Aim To observe the effects of Wenfei Jiangzhuo formula(WFJZF)on rats with vascular de-mentia and investigate its possible mechanism of ac-tion.Methods Thirty-six healthy male SD rats were randomly divided into the sham group,model group,donepezil group,and low-dose,medium-dose and high-dose groups of Wenfei Jiangzhuo formula,with six rats per group.Except for the sham group,the other groups were prepared as VaD models,and each group was gavaged with the corresponding drugs after suc-cessful modeling,and tests were performed after three weeks of treatment.Behavioral,hippocampal CA1 area morphology,neural dendrites and mitochondrial chan-ges were observed in all groups of rats,and phospho-glycerate mutase 5(PGAM5),dynamics-related pro-teins1(Drp1),opticatrophyprotein-1(OPA1),and other proteins were detected in each group.Results Compared with the sham group,rats in the model group and each intervention group had prolonged es-cape latency(P＜0.05),a shorter number of travers-als across the platforms(P＜0.05),a sparse morphol-ogy of hippocampal neurons,a reduction in the number of secondary dendritic spines,and a rupture of the out-er membrane of the mitochondria;the expression of the PGAM5 and Drp1 proteins in hippocampal tissues was elevated(P＜0.05),and the expression of the OPA1 and Mfn1/2 protein expression decreased(P＜0.05);compared with the model group,donepezil group and Wenfei Jiangzhuo formula high-dose group of rats had shorter evasion latency(P＜0.05),increased number of times to traverse the platform(P＜0.05),increased number of hippocampal neurons,tightly packed,more secondary dendritic structures,and reduced mitochon-drial damage;the expression of PGAM5 and Drp1 pro-teins was reduced(P＜0.05),and the expression of OPA1 and Mfn1/2 proteins was elevated(P＜0.05).Conclusions Wenfei Jiangzhuo formula can regulate the PGAM5-Drp1 signaling axis to improve the balance of mitochondrial homeostasis,thus improving the cog-nitive condition of the brain and exerting cerebroprotec-tive effects.

Purpose To explore the value of contrast-enhanced ultrasound(CEUS)in the differential diagnosis of gallbladder polypoid lesions(GPLs)(diameter≥10 mm).Materials and Methods A prospective enrollment of 229 patients with GPLs who underwent cholecystectomy in 17 hospitals from December 1 2021 to June 30 2024 was conducted to analyze the relationship between general data,conventional ultrasound,CEUS characteristics and the nature of GPLs.Multivariate Logistic regression was employed to identify independent risk factors for neoplastic polyps,the differential diagnostic value of different indicators was compared.Results Among 229 patients with GPLs,there were 108 cases of cholesterol polyps,102 cases of adenoma and 19 cases of gallbladder cancer.Age(Z=-4.476,P<0.001),polyp number(χ2=15.561,P<0.001),diameter(Z=-8.149,P<0.001),echogenicity(χ2=9.241,P=0.010),vascularity(χ2=23.107,P<0.001),enhancement intensity(χ2=47.610,P<0.001),enhancement pattern(χ2=6.468,P=0.011),vascular type(χ2=84.470,P<0.001),integrity of gallbladder wall(χ2=7.662,P=0.006)and stalk width(Z=-9.831,P<0.001)between cholesterol polyps and neoplastic polyps were statistically significant.Age,location,diameter,echogenicity,enhancement pattern,vascular type and stalk width between adenoma and gallbladder cancer were statistically significant(Z=-4.333,-3.902,-5.042,all P<0.05).Multivariate Logistic regression analysis showed that hyper-enhancement,branched vascular type and stalk width were independent risk factors for neoplastic polyps(OR=4.563,5.770,3.075,all P<0.001).The combination of independent risk factors was better than single factor and diameter in the differential diagnosis of cholesterol polyps and neoplastic polyps(all P<0.01).Conclusion CEUS can effectively identify the nature of GPLs and provide a valuable imaging reference for the selection of treatment methods.

Objective:To investigate the expression of microRNA-27b (miRNA-27b) , miRNA-221 and miRNA-222 in keloids and their relationship with vascular endothelial growth factor (VEGF).Methods:From January 2021 to January 2022, 36 cases of keloid tissue (keloid group) , 36 cases of normal adjacent scar tissue (normal control group) and 12 cases of flat scar (flat scar group) were selected from Dermatology and Venereology Department of Xinjiang Uygur Autonomous Region People’ s Hospital. VEGF protein expression and microvascular density in the three groups were determined by immunohistochemistry, and the expression levels of miRNA-27b, miRNA-221 and miRNA-222 were detected by real-time quantitative PCR. SPSS 27. 0 statistical software was used for analysis. The measurement data of normal distribution were expressed as Mean ± SD. ANOVA was used for multi-group comparison, and LSD method was used for pound-for-pair multiple comparison. The measurement data of non-normal distribution were expressed as M ( Q1, Q3) , and Kruskal-Wallis H test was used for comparison between groups. Spearman correlation analysis was used for correlation analysis among data. All tests were bilateral tests, and P<0. 05 was considered statistically significant. Results:The levels of VEGF protein and microvascular count in keloid group [(0. 28±0. 08) , (47. 78±14. 06) bar/×400 view] were significantly higher than those in normal control group [(0.09±0.05), (10.25±5.08) bar/×400 view] and flat scar group [(0.19±0.06) , (23.75±7.94) bar/× 400 view] , the difference was statistically significant ( P < 0. 01) . The expression level of miR-27b in keloid group [0.50 (0.32, 0.64) ] was significantly lower than that in normal control group [0.69 (0.37, 1.69) ] and flat scar group [1.35 (0.68, 1.74) ] , the difference was statistically significant ( P<0. 05). There were no significant difference in the expression levels of miR-221 and miR-222 among the three groups ( P>0. 05 ). Correlation analysis showed that miR-27b, miR-221, miR-222 were positively correlated with VEGF protein expression in keloid group ( r=0.36, 0.41, 0.37, P<0. 05). Conclusions:miR-27b, miR-221 and miR-222 in keloid are positively correlated with the expression of VEGF, which may have certain regulatory effects on its angiogenesis, and the low expression of miR-27b may play an important role in the occurrence and development of keloid.

Objective:To investigate the expression of microRNA-27b (miR-27b), miR-221 and miR-222 in keloids and their relationships with vascular endothelial growth factor (VEGF).Methods:From January 2021 to January 2022, 36 cases of keloid tissue (keloid group), 36 cases of adjacent normal tissue (normal control group) and 12 cases of flat scars (flat scar group) were collected from Dermatology and Venereology Department of Xinjiang Uygur Autonomous Region People's Hospital. VEGF protein expression and microvessel density in the three groups were determined by immunohistochemistry, and the expression levels of miR-27b, miR-221 and miR-222 were detected by real-time quantitative PCR. SPSS 27.0 statistical software was used for statistical analysis. The normally distributed measurement data were expressed as Mean±SD. ANOVA was used for multi-group comparison, and the LSD method was used for pound-for-pair multiple comparisons. The measurement data of non-normal distribution were expressed as M ( Q1, Q3), and Kruskal-Wallis H test was used for the comparison between groups. Spearman correlation analysis was used for the correlation analysis among data. All tests were bilateral tests, and P<0.05 was considered statistically significant. Results:The levels of VEGF protein and microvessel count in the keloid group [0.28±0.08, (47.78±14.06) bar /×400 view] were significantly higher than those in normal control group [0.09±0.05, (10.25±5.08) bar /×400 view] and flat scar group [0.19±0.06, (23.75±7.94) bar /×400 view], the difference was statistically significant ( P<0.01). The expression level of miR-27b in keloid group [0.50 (0.32, 0.64)] was significantly lower than that in normal control group [0.69 (0.37, 1.69)] and flat scar group [1.35 (1.25, 1.74)], the difference was statistically significant ( P<0.01). There were no significant differences in the expression levels of miR-221 and miR-222 among the three groups ( P>0.05). Correlation analysis showed that miR-27b, miR-221, miR-222 were positively correlated with VEGF protein expression in keloid group ( r=0.36, 0.41, 0.37, P<0.05). Conclusion:The expression of miR-27b is different in keloid, flat scar and normal tissue. miR-27b, miR-221 and miR-222 are positively correlated with VEGF expression in keloid, suggesting that the miRNA/VEGF axis may play a key role in the occurrence and progression of keloid.

Objective:To investigate the expression of microRNA-27b (miRNA-27b) , miRNA-221 and miRNA-222 in keloids and their relationship with vascular endothelial growth factor (VEGF).Methods:From January 2021 to January 2022, 36 cases of keloid tissue (keloid group) , 36 cases of normal adjacent scar tissue (normal control group) and 12 cases of flat scar (flat scar group) were selected from Dermatology and Venereology Department of Xinjiang Uygur Autonomous Region People’ s Hospital. VEGF protein expression and microvascular density in the three groups were determined by immunohistochemistry, and the expression levels of miRNA-27b, miRNA-221 and miRNA-222 were detected by real-time quantitative PCR. SPSS 27. 0 statistical software was used for analysis. The measurement data of normal distribution were expressed as Mean ± SD. ANOVA was used for multi-group comparison, and LSD method was used for pound-for-pair multiple comparison. The measurement data of non-normal distribution were expressed as M ( Q1, Q3) , and Kruskal-Wallis H test was used for comparison between groups. Spearman correlation analysis was used for correlation analysis among data. All tests were bilateral tests, and P<0. 05 was considered statistically significant. Results:The levels of VEGF protein and microvascular count in keloid group [(0. 28±0. 08) , (47. 78±14. 06) bar/×400 view] were significantly higher than those in normal control group [(0.09±0.05), (10.25±5.08) bar/×400 view] and flat scar group [(0.19±0.06) , (23.75±7.94) bar/× 400 view] , the difference was statistically significant ( P < 0. 01) . The expression level of miR-27b in keloid group [0.50 (0.32, 0.64) ] was significantly lower than that in normal control group [0.69 (0.37, 1.69) ] and flat scar group [1.35 (0.68, 1.74) ] , the difference was statistically significant ( P<0. 05). There were no significant difference in the expression levels of miR-221 and miR-222 among the three groups ( P>0. 05 ). Correlation analysis showed that miR-27b, miR-221, miR-222 were positively correlated with VEGF protein expression in keloid group ( r=0.36, 0.41, 0.37, P<0. 05). Conclusions:miR-27b, miR-221 and miR-222 in keloid are positively correlated with the expression of VEGF, which may have certain regulatory effects on its angiogenesis, and the low expression of miR-27b may play an important role in the occurrence and development of keloid.