Objective: The aim of this study was to explore the effects of Babao dan (BBD), a traditional Chinese medicine, on gastric cancer (GC) progression in vivo . Materials and Methods: A subcutaneous xenograft mouse model of GC was established using MGC80-3 cells. The terminal deoxynucleotidyl transferase-mediated dUTP: 2’-deoxyuridine 5’-triphosphate -biotin nick-end labeling method was adopted to detect cell apoptosis in vivo . The expression levels of proteins associated with proliferation, apoptosis, and angiogenesis were measured by immunohistochemical staining or western blotting (WB). The activation and protein levels of p-c-Jun N-terminal kinase (JNK), p-p38, p-extracellular-regulated kinase 1/2, p-nuclear factor-κB (NF-κB), and p-STAT3 were examined by Bio-plex and WB. Results: BBD significantly inhibited tumor growth in GC mouse models with no adverse effect on body weight or organ function. It was also found that BBD significantly suppressed the proliferation of GC tumor cells, induced the apoptosis of tumor cells, and inhibited angiogenesis through inactivating with mitogen-activated protein kinase, NF-κB, and STAT3 pathways. Conclusions: BBD exerts suppressive effects on GC tumor growth by regulating multiple pathways in vivo , which may provide a novel treatment option for GC therapy.

[Abstract]: Objective: To observe the effects of ursolic acid (UA) on the apoptosis, autophagy and mTOR of human colorectal cancer (CRC) cells resistant to 5-FU (HCT-8/5-FU), and explore the mechanisms of UA reversing the multidrug resistance (MDR) of CRC. Methods: HCT-8 cells and its resistant cells to 5-FU (HCT-8/5-FU) were cultured to calculate the resistant index and confirmed the resistance of HCT-8/5-FU. The MTT assays were used to screen the suitable concentrations and the reversal fold of UA. The efflux function, proliferation, apoptosis, autophagy and their correlated proteins were determined through Doxorubucin staining, Rhodamine 123 staining, colony formation, Annexin V-PI double staining, Cyto-ID staining and Western blot after the HCT-8/5-FU were intervened with UA for 48 h. Results: HCT-8/5-FU cells are resistant to different chemotherapeutics, UA could reverse the MDR effectively. Furtherly, UA down-regulates the expression of ABCB1, ABCG2, p62, up-regulates Bax/Bcl-2 and LC3II/LC3I to inhibit the drug-efflux (P<0.05) and induce the apoptosis (P<0.05) and autophagy (P<0.05) via inhibiting the phosphorylation of mTOR. Conclusion: UA induces the apoptosis and autophagy, blocks the proliferation of HCT-8/5-FU cells via inhibiting the phosphoralation of mTOR, that maybe the important mechanism by which UA reverses the MDR of CRC.

Gastric cancer (GC) is one of the most common gastrointestinal malignancies in the world. Growing evidence emphasizes the critical role of long non-coding RNA (lncRNA) in GC tumorigenesis. The aim of the research was to elucidate the effect and mechanism of Babao Dan (BBD) on lymphangiogenesis of GC in vitro and in vivo via lncRNA-ANRIL/VEGF-C/VEGFR-3 signaling axis. The present study investigated BBD significantly decreased the expression of lncRNA-ANRIL and VEGF-C in GC cells (AGS, BGC823, and MGC80-3) by using real-time quantitative polymerasechain reaction (RT-qPCR) and the secretion and expression of VEGF-C by (enzyme linked immunosorbent assay) ELISA and western blot (WB). BBD significantly inhibited the tumor xenograft of GC growth and the expression of lncRNA-ANRIL, VEGF-C, VEGFR-3 and LYVE-1 in vivo. BBD reduced serum VEGF-C level. In vitro, BBD inhibited the tube formation and decreased the cell viability, proliferation and migration of HLECs by using tube formation, MTT, Hoechst and Transwell assays. In addition, WB assay found that BBD decreased the expression levels of VEGF-C, VEGFR-3, matrix metallopeptidase 2 (MMP-2) and matrix metallopeptidase 9 (MMP-9), and RT-qPCR assay found that the mRNA expression levels of lncRNA-ANRIL, VEGF-C, VEGFR-3, MMP-2, MMP-9, CDK4, Cyclin D1, and Bcl-2 were down-regulated, and the expression of p21 and Bax were increased. Taken together, these results demonstrated that BBD inhibited lymphangiogenesis of GC in vitro and in vivo via the lncRNA-ANRIL/VEGF-C/VEGFR-3 signaling axis.

Background Anlotinib is a multi-tyrosine kinase inhibitor that has been reported to have activity against colorectal cancer. However, the functional mechanisms whereby anlotinib mediates against deadly drug-resistant colorectal cancer (CRC) has not been fully described-specifically, the potential mechanisms that inhibit proliferation and induce apoptosis remain largely unknown. Methods MTT assays were used to detect cell viability and calculate the resistance index. Colony formation was used to evaluate the proliferation of resistant cells. DAPI staining was used to detect cell apoptosis morphologically. Annexin V-FITC with PI staining was used to detect early and late-stage apoptosis of cells. Cell cycle distribution was determined by Flow cytometry. Transwell assays were performed to examine the ability of migration and invasion. Cyclin D1 Survivin, CDK4, Bcl-2, Bax and changes of PI3K/AKT pathway were detected by Western blotting. Compared as a single agent or combined with anlotinib or LY294002, PI3K inhibitor (LY294002) was used to verify whether it inhibited drug-resistant CRC cells by lowering PI3K/AKT. Results HCT-8/5-FU cells showed multiple drug resistance. Drug resistance index of 5-FU, ADM and DDP were 390.27, 2.55 and 4.57, respectively. Anlotinib was shown to inhibit cell viability on HCT-8/5-FU and HCT-8 cells for 24 h and 48 h in a dosage- and time-dependent pattern. Compared with 48 h, intervened with anlotinib (0 μM, 10 μM, 20 μM and 40 μM) for 24 h, the HCT-8/5-FU cells were sensitive to anlotinib, and their sensitivity was greater than that of the parent cell line (HCT-8) at 24 h. Further, anlotinib inhibited the number of cloned cells significantly and had a significant inhibitory effect on cell cycle, mainly by blocking G1 transferring to S phase. Moreover, anlotinib could down-regulate the expression of survivin, cyclin D1, CDK4, caspase-3, Bcl-2, MMP-2, vimentin, MMP-9, and N-cadherin, while up-regulating cleaved-caspase-3, Bax and E-cadherin. Anlotinib inhibited the activity of the PI3K/AKT pathway and induced apoptosis in HCT-8/5-FU cells. Using LY294002, a specific PI3K inhibitor, our experiment found anlotinib can inhibit drug-resistant CRC cells by reducing PI3K and p-AKT activity-induce apoptosis. Conclusions Anlotinib inhibited the proliferation, metastasis and induced apoptosis of HCT-8 / 5-FU cells; and the mechanism could be that anlotinib overcomes multiple drug resistant of the colorectal cancer cells via inactivating PI3K/AKT pathway.

目的:探讨解毒消癥饮(JXY)对血管生成因子A(VEGFA)诱导的人脐静脉内皮细胞(HUVECs)凋亡、迁移以及血管生成的体外影响.方法:HUVECs分为对照组、诱导组(VEGFA 10ng/mL)、JXY低剂量组(VEGFA10ng/L+JXY 0.05mg/mL)、JXY中剂量组(VEGFA 10ng/mL+JXY 0.1mg/mL)、JXY高剂量组(VEGFA10ng/mL+JXY 0.2mg/mL),通过MTT、Hoechst、划痕实验,管腔形成实验、Transwell以及Western blot分别检测细胞活力、凋亡、修复能力、血管生成、细胞迁移和VEGFR2、MMP2、MMP9蛋白表达.结果:与诱导组比较,JXY以剂量依赖性地抑制VEGFA诱导的细胞增殖、修复能力,迁移以及体外管腔的形成能力(P＜0.01),促进凋亡(P＜0.05,P＜0.01).进一步研究表明JXY剂量依赖性降低VEGFR2、MMP2、MMP9蛋白表达量.结论:JXY显著抑制VEGFA诱导的HUVECs细胞体外血管生成,与其降低VEGFR2、MMP2、MMP9表达直接相关.

目的 探讨清解扶正颗粒(Qingjie Fuzheng Granules,QFG)对血管生成因子A(vascular endothelial growth factor,VEGF-A)诱导的肿瘤血管生成的抑制作用及其作用机制.方法 体外培养肠癌细胞HCT-8、肝癌细胞Huh7和胃癌细胞MGC80-3,经不同剂量(0、0.25、0.5、1、1.5、2 mg/mL)QFG干预处理后,用MTF法检测细胞活力,Western blot实验检测VEGF-A蛋白表达;体外培养脐静脉血管内皮细胞(HUVECs),HUVECs分为对照组、诱导组(VEGF-A 10 ng/mL)、VEGF-A 10 ng/mL+QFG 0.5 mg/mL组、VEGF-A 10ng/mL+QFG 1 mg/m L组和VEGF-A 10 ng/mL+QFG 2 mg/mL组,通过MTT、DAPI染色、划痕实验、Transwell实验,管腔形成及Western blot实验分别检测细胞活力、凋亡、迁移、血管生成和VEGFR-2蛋白表达.结果 QFG可以抑制肠癌细胞HCT-8、肝癌细胞Huh7和胃癌细胞MGC80-3的细胞活力以及蛋白VEGF-A的表达,且具有统计学差异;QFG能够抑制VEGF-A诱导HUVECs的增殖,促进细胞凋亡,抑制其损伤修复、迁移及管腔生成能力,也可以下调蛋白VEGFR-2的表达水平,具有统计学差异.结论 QFG可靶向VEGF-A抑制肿瘤血管生成.

Background: Sonic Hedgehog (SHh) signaling pathway plays a critical role in cell proliferation, apoptosis, and tumor angiogenesis in various types of malignancies including colorectal cancer (CRC). Qingjie Fuzheng Granules (QFG) is a traditional Chinese medicinal formula, which has been clinically used in various cancer treatments, including CRC. In this study, we explored the potential molecular mechanisms of QFG treatment effects on CRC via the SHh pathway. Methods: A CRC HCT-116 xenograft mouse model was utilized for all experiments. Mice were treated with intra-gastric administration of 1 g/kg of QFG or saline 6 days a week for 28 days (4 weeks). Body weight, length and shortest diameter of the tumor were measured every 3 days. At the end of the treatment, the tumor weight was measured. TUNEL staining assays were used to detect tumor apoptosis. Western blot and immunohistochernistry (IHC) assays were used to detect the expression of relative proteins. Results: In our results, QFG inhibited the increase of tumor volume and weight, and exhibited no impact on mouse body weight. Furthermore, QFG significantly decreased the expression of SHh, Smo and Gli proteins, indicating the action of SHh signaling. Consequently, the expression of pro-proliferative survivin, Ki-67, Cyclin-D1 and CDK4 were decreased and expression of anti-proliferative p21 was increased. The pro-apoptotic Bax/Bcl-2 ratio, cle-caspase-3 and TUNEL-positive cell percentage in tumor tissues were increased. Meanwhile, the pro-angiogenic VEGF-A and VEGFR-2 expression was down-regulated. Conclusions: QFG inhibited CRC cell proliferation and promoted CRC cell apoptosis and tumor angiogenesis in vivo through the suppression of SHh pathway, suggesting that QFG could be a potential therapeutic drug for CRC.

Background: Clinical studies and biological mechanism research showed that Babao Dan (BBD) exerts strong activity against many types of cancer, including gastric cancer (GC). in this article, the effect of BBD on proliferation of human gastric cancer cells (AGS, MGC80-3) was studied. Methods: AGS and MGC80-3 cells were treated with various concentrations of BBD in vitro. The cell viability and survival rate were determined by the MTT assay and colony formation assay. The cell cycle analysis was measured by PI staining with flow cytometry. The level of G1/S phase check point related proteins (p53, p-p53, PCNA, Survivin, Cyclin Dl, CDK4, p21) were determine by Western Blot. Results: BBD inhibited AGS and MGC80-3 cells viability and decreased survival rate in a dose-dependent manner. The percentage of S-phase of AGS and MGC80-3 were found to be significant decreased in dose-dependent manner after cells were treated by different concentration BBD for 24 h. In addition, increased BBD concentration up-regulated protein p-p53, p21 level and down-regulated the expression of cell survival key protein Survivin, cell proliferation key protein PCNA and cell cycle related protein Cyclin D1, CDK4, which is closely correlated with the G1/S phase checkpoint. Conclusion: BBD is likely to inhibit the proliferation of gastric cancer cells with blocking G1/S cell cycle transition by regulating the p53 pathway. Thus, BBD may become a promising agent used for GC clinical treatment. Copyright (C) 2020, Taiwan Society of Geriatric Emergency & Critical Care Medicine.

目的:通过对比肝癌亲本Bel-7402细胞及其5-FU耐药Bel-7402/5-FU细胞中微小RNA (microRNA,miRNA)的表达差异,探讨miRNA在肝癌细胞多药耐药中的作用.方法:体外培养Bel-7402细胞及其耐药株Bel-7402/5-FU细胞,MTT法检测Bel-7402/5-FU细胞对不同化疗药物的敏感性,miRNA表达芯片检测Bel-7402细胞和Bel-7402/5-FU细胞miRNA的差异表达,qPCR验证差异表达的miRNA.结果:Bel-7402/5-FU细胞对不同的化疗药物均具有耐药性;miRNA芯片检测结果发现,耐药株Bel-7402/5-FU细胞与亲本Bel-7402细胞中,差异表达的miRNA有29个,其中上调14个,下调15个;qPCR验证结果发现,和亲本Bel-7402细胞比较,耐药株Bel-7402/5-FU细胞中miR-10a-5p、-371 a-3p、-371 a-5p、-372,-373-3p、-146-5p、-6723-5p显著下调,miR-4497、-3148显著上调.结论:肝癌多药耐药的发生与miRNA表达异常有关.

Objective The objective was to further investigate apoptosis induction by Babao Dan (BBD), which supports its anti-tumor mechanisms, using two human gastric cancer cell lines (AGS and MGC80-3). Methods After treatment with various BBD concentrations, cell viability and cytotoxic effects were investigated using methyl thiazolyl tetrazolium (MTT) and lactate dehydrogenase (LDH) assays, respectively. The following indicators of cell apoptosis were evaluated: Annexin V-APC staining, caspase-3/-8/-9 activation, and mitochondrial membrane potential loss. Apoptosis-related protein levels (including Bcl-2-associated X protein [Bax], B-cell CLL/lymphoma 2 [Bcl-2], factor associated suicide [Fas], and Fas ligand [FasL]) were determined by western blot. The following multi-pathway factors were also assessed: p-ERK1/2, p-JNK, p-p38, and p-NF-κB. Results The MTT and LDH assays both demonstrated increased BBD cytotoxicity. BBD induced cell apoptosis by stimulating caspase-3/-8/-9 activity and destroying the mitochondrial membrane potential. BBD also regulated key factor expression levels including Bcl-2, Bax, Fas, and FasL and down-regulated protein phosphorylation via the MAPK and NF-κB pathway. Conclusions The possible anti-tumor mechanism is that BBD induces apoptosis via the MAPK and NF-κB signaling pathways.

Crohn's disease may cause excessive damage and repair in the intestinal epithelium due to its chronic relapsing intestinal inflammation. These factors may initiate the TGF-β 1-Smad pathway to activate the transcription factor of Snail, and the Snail-mediated pathway promotes the transformation of intestinal epithelial cells to mesenchymal cells, leading to intestinal fibrosis. Acupuncture and moxibustion have been demonstrated to prevent intestinal fibrosis in Crohn's disease. However, it is not clear whether acupuncture and moxibustion can inhibit intestinal epithelial mesenchymal transformation in Crohn's disease by affecting the TGF-β 1-Smad-Snail pathway. This study indicated that abnormal increased expressions of TGFβ1, TβR2, Smad3, and Snail were significantly downregulated by herbs-partitioned moxibustion at Tianshu (ST25) and Qihai (RN6) and acupuncture at Zusanli (ST36) and Shangjuxu (ST37). In addition, protein and mRNA levels of E-cadherin, the epithelial cell marker, were significantly increased. Protein and mRNA levels of fibronectin, the mesenchymal cell marker, were decreased in the intestinal tissue. Moreover, the number of mesenchymal cells in the intestinal mucosa can be reversely transformed to intestinal epithelial cells. Therefore, herbs-partitioned moxibustion combined with acupuncture can prevent intestinal epithelial mesenchymal transition by inhibiting abnormal expression of TGFβ1, TβR2, Smad3, and Snail in the TGF-β1-Smad-Snail pathway in Crohn's disease.

BACKGROUND Qingjie Fuzheng granules (QFGs) are part of a traditional Chinese medicine formula, which has been widely used and found to be clinically effective with few side effects in various cancer treatments, including colorectal cancer (CRC). However, the precise mechanisms and molecular signaling pathways involved in the activity of QFGs' anticancer effect have not been reported in the literature. In this study, we hypothesized that QFGs can inhibit the growth of colorectal cancer cells, and that its mechanism is closely related to one or more intracellular signal transduction pathways. AIM To better evaluate the mechanism underlying the anti-cancer effect of QFGs on the CRC cell lines HCT-116 and HCT-8. METHOD First, we measured cell viability and cytotoxicity by performing MTT and lactate dehydrogenase (LDH) assays. We evaluated the role of QFGs in cell proliferation and apoptosis by assessing colony formation and analyzing Hoechst 33258 staining. Second, cell cycle and apoptosis rates were measured by fluorescence activated cell sorting, and the expression levels of survivin, cyclin D1, CDK4, p21, Bax, Bcl-2, Fas, FasL, and cleaved-caspase-3/-8/-9 were measured by performing western blots and caspase activity assays. Furthermore, inhibitors of caspase-3/8/-9 were used to elucidate the specific apoptosis pathway induced by QFGs in cancer cells. Finally, activation of the PI3K/AKT and ERK signaling pathways was examined using the western blot assay to investigate the possible mechanism. RESULTS MTT and LDH assays revealed that after 0.5-2.0 mg/mL of QFGs treatment, cell viability was reduced by (6.90% +/- 1.03%)-(59.70% +/- 1.51%) (HCT-116; P < 0.05) and (5.56% +/- 4.52%)-(49.44% +/- 2.47%) (HCT-8; P < 0.05), and cytotoxicity was increased from 0.52 +/- 0.023 to 0.77 +/- 0.002 (HCT-116; P < 0.01) and from 0.56 +/- 0.054 to 0.81 +/- 0.044 (HCT-8; P < 0.01) compared with the non-QFGs treatment groups. Additionally, colony formation and Hoechst 33258 staining assays showed that QFGs inhibited proliferation and induced apoptosis in CRC cells. QFGs also increased the expression levels of Bax, Fas and FasL, decreased the level of Bcl-2, and stimulated the activation of caspase-3/-8/-9, which were revealed by western blot and caspase activity assays. In contrast, when adding the three caspase inhibitors, the suppression effect of QFGs on cell viability and apoptosis were markedly inhibited. Moreover, QFGs suppressed the phosphorylation levels of PI3K, AICT and ERK. CONCLUSION These results demonstrated that QFGs can inhibit CRC cell proliferation and induce apoptosis by suppressing the PI3K/AKT and ERK signaling pathways.

目的 探讨八宝丹(BBD)对胃癌细胞转移的影响. 方法 体外培养胃癌细胞AGS和MGC803,予不同剂量(0.25、0.5、0.75 mg/mL) BBD干预处理.采用MTT法检测细胞的活力,划痕实验观察细胞的损伤修复能力,Transwell实验观察细胞的迁移能力,粘附实验观察细胞的粘附能力. 结果 BBD可抑制AGS和MGC803细胞的活力,抑制细胞的损伤修复能力,抑制细胞的迁移能力,抑制细胞的粘附能力,均呈现明显的剂量依赖作用. 结论 BBD对胃癌细胞的迁移能力具有显著抑制作用,提示BBD可抑制胃癌细胞的转移.

目的 探讨八宝丹(BBD)对人胃癌细胞增殖与凋亡的影响. 方法 体外培养胃癌细胞AGS和MGC-803,采用不同浓度的BBD(0、0.25、0.5、0.75、1mg/mL)进行干预,MTT法检测细胞活力,计算BBD对细胞增殖的抑制率;倒置显微镜观察细胞生长密度;台盼蓝染色法检测细胞数量;细胞集落形成实验检测细胞集落形成能力;Hoechst染色检测细胞凋亡. 结果 BBD可显著抑制胃癌细胞AGS和MGC-803的细胞活力,抑制细胞增殖,使细胞密度下降,减少细胞数量,抑制细胞集落形成能力,诱导细胞凋亡. 结论 BBD可显著抑制胃癌细胞AGS和MGC-803的增殖及诱导细胞凋亡.

AIM To observe whether there are differences in the effects of electro-acupuncture (EA) and moxibustion (Mox) in rats with visceral hypersensitivity. METHODS EA at 1 mA and 3 mA and Mox at 43 °C and 46 °C were applied to the Shangjuxu (ST37, bilateral) acupoints in model rats with visceral hypersensitivity. Responses of wide dynamic range neurons in dorsal horns of the spinal cord were observed through the extracellular recordings. Mast cells (MC) activity in the colons of rats were assessed, and 5-hydroxytryptamine (5-HT), 5-hydroxytryptamine 3 receptor (5-HT3R) and 5-HT4R expressions in the colons were measured. RESULTS Compared with normal control group, responses of wide dynamic range neurons in the dorsal horn of the spinal cord were increased in the EA at 1 mA and 3 mA groups (1 mA: 0.84 ± 0.74 vs 2.73 ± 0.65, P < 0.001; 3 mA: 1.91 ± 1.48 vs 6.44 ± 1.26, P < 0.001) and Mox at 43 °C and 46 °C groups (43 °C: 1.76 ± 0.81 vs 4.14 ± 1.83, P = 0.001; 46 °C: 5.19 ± 2.03 vs 7.91 ± 2.27, P = 0.01). MC degranulation rates and the expression of 5-HT, 5-HT3R and 5-HT4R in the colon of Mox 46 °C group were decreased compared with model group (MC degranulation rates: 0.47 ± 0.56 vs 0.28 ± 0.78, P < 0.001; 5-HT: 1.42 ± 0.65 vs 7.38 ± 1.12, P < 0.001; 5-HT3R: 6.62 ± 0.77 vs 2.86 ± 0.88, P < 0.001; 5-HT4R: 4.62 ± 0.65 vs 2.22 ± 0.97, P < 0.001). CONCLUSION The analgesic effects of Mox at 46 °C are greater than those of Mox at 43 °C, EA 1 mA and EA 3 mA.

To evaluate and compare electroacupunctures (EA) with different parameters and moxibustion at different temperatures influencing the activation of mast cells (MC) in Tianshu (ST 25) regions of visceral hyperalgesia model rats.

OBJECTIVE:To compare the effects of electroacupuncture (EA) and moxibustion (Moxi) on visceral pain and expression of vanilloid receptor subtype 1 (VR 1) and heat shock protein (HSP)70 in "Tianshu" (ST 25) region in colorectal distension (CRD)-induced visceral hypersensitivity (VHS) rats. METHODS:Fifty male SD rats were randomly divided into normal control, VHS model, 43℃-moxi, 46℃-moxi, 1 mA-EA and 3 mA-EA groups (n=10 in each group). The VSH model was established by CRD once daily for 14 days. EA or Moxi stimulation was applied to bilateral "Tianshu" (ST 25) for 10 min, once daily for consecutive 10 days. The abdominal withdrawal reflex (AWR) scores (0-4 points) were rated according to Al-Chaer's and coworkers' standards (2000) and the expression levels of VR 1 and HSP 70 in bilateral ST 25 area tissues detected by immunohistochemistry. RESULTS:The AWR scores for 20, 40, 60 and 80 mmHg CRD pressures were significantly increased compared to the normal control group (P<0.01) and notably decreased after 43℃- and 46℃-moxi, and 1 mA- and 3 mA-EA stimulation of bila-teral ST 25 in comparison with the model group (P<0.05, P<0.01), and the effect of 46℃-moxi was apparently superior to those of 1 mA-EA at 40 and 80 mmHg, and 3 mA-EA at 40 mmHg (P<0.05). After modeling, the expression of both VR 1 and HSP 70 (percentages of area of positive-cells) in ST 25 region had no significant changes (P>0.05). Compared to the model group, the expression levels of VR 1 in the 43℃-moxi and 46℃-moxi groups, and HSP 70 in the 43℃-moxi and 46℃-moxi, 1 mA-EA and 3 mA-EA groups were significantly up-regulated (P<0.01), but without obvious changes in the expression of VR 1 in the 1 mA-EA and 3 mA-EA groups (P>0.05). The effects of 46℃-moxi were considerably better than those of 43℃-moxi, 1 mA-EA and 3 mA-EA in up-regulating VR 1 and HSP 70 expression (P<0.05, P<0.01). No significant differences were found among the 43℃-moxi, 1 mA-EA and 3 mA-EA groups in the expression of VR 1 and HSP 70 (P>0.05). CONCLUSIONS:Moxibustion at 43℃ and 46℃ and EA at 1 mA and 3 mA, especially the 46℃-moxi, can relieve visceral pain in visceral hypersensitivity rats, which may be related to their effects in up-regulating expression of VR 1 and HSP 70 in "Tianshu" (ST 25) area.

The clinical experience of professor SHI Yin for polycystic ovary syndrome (PCOS) was summarized. According to the main pathogenesis of PCOS, the tonifying kidney should be taken as essence with synchronous treatment on liver, spleen and heart, presenting staging, classification and sorting method for PCOS. In the staging method, the regulation on follicle development should be taken as treatment core to comply with the rules of yin and yang. A four-stage method was proposed, where "regulating method" was suitable in menstrual period, "tonifying method" in follicular phase;"dredging method" in ovulatory period and "adjustment and tonifying " in luteal phase. In the classification and sorting method, attention was paid on individualized treatment, and treatment was based on fat type, thin type and non-fat type as well as childbearing. Besides, psychological counseling and life adjustment for patient was essential, and the unity of body and mind could enhance curative effect.

Herb-partitioned moxibustion (HPM) at Tianshu (ST25) and Qihai (RN6) has been used to treat Crohn’s disease (CD). Injury to intestinal epithelial tight junctions (TJs) is the leading cause of CD onset with under expression of TJ-related proteins such as occludin, claudin-1, and zonula occludens protein-1 (ZO-1). This study aimed to investigate whether HPM can change the permeability of the intestinal epithelial barrier by affecting the expression of colonic epithelial TJ-related proteins in vitro.

Jiujing Tu (Illustration of Moxibustion), excavated from Mo Kao Grotto at Dunhuang, is one of the earliest existing monographs on moxibustion. The medical masters from different schools have focused on this book because it is different from the existing ancient medical works and have not been collected in the medical works of different dynasties. In this study, the literature of Jiujing Tu on five acupoints (Dachangshu, Pangguangshu, Daxiaochangshu, Nieshu and Cigong) relevant with intestinal disorders is collected. It is intended to discuss and analyze the acupoint location, main intestinal disorder, moxibustion characters, recognition on the literature of different dynasties and modern clinical applications. It is believed that the thought of strong moxibustion in the treatment of intestinal disorders advocated in Jiujing Tu has profound impact on the medical development in later generations. It deserves us to have a further digging, collection and promotion of this thought in the modern time.