OBJECTIVE: To evaluate the effects of madecassoside (MC) on the depression behavior of mice and the activities of monoamine oxidase (MAO) in different rat brain regions. METHODS: Imipramine as the positive contrast medicine, effects of MC on the depression behavior of mice were observed by forced swimming test and reserpine antagonist test. Moclobemide and pargyline as the positive controlled medicines, the activities of monoamine oxidase-A (MAO-A) and monoamine oxidase-B (MAO-B) in different rat brain regions were determined after intragastric administration of MC in 3 different dosages for 3 days or 21 days. RESULTS: (1) The low, middle and high dosages of MC (i.g.) significantly reduced the immobility time of mice in forced swimming test (P<0.05). (2) MC in dosages of 10 mg/kg and 20 mg/kg prevented the lowering of temperature induced by reserpine (P<0.05), while 40 mg/kg had no significant effects on it (P>0.05). (3) With acute administration (3 days), the low, middle and high dosagey of MC (i.g.) significantly inhibited the activity of MAO-A in hippocampus (P<0.01), and the high dosage significantly inhibited the activity of MAO-A in hypothalamus (P<0.01), while the 3 dosages had no significant effects on the activity of MAO-A in cortex (P>0.05). With chronic administration (21 days), MC in 3 dosages had no significant effects on the activities of MAO-A in cortex and hypothalamus (P>0.05), and the high dosage (40 mg/kg) significantly enhanced the activity of MAO-A in hippocampus (P<0.01). (4) With acute administration, MC in dosages of 10 mg/kg and 20 mg/kg significantly inhibited the activity of MAO-B in cortex (P>0.05), and MC in dosage of 10 mg/kg significantly inhibited the activity of MAO-B in hypothalamus (P<0.05), and MC in dosage of 20 mg/kg significantly enhanced the activity of MAO-B in hippocampus (P<0.01). With chronic administration, MC of 3 dosages produced no significant effects on the activities of MAO-B in 3 different rat brain regions (P>0.05). CONCLUSION: These results support the idea that MC produces antidepressant effects through MAO inhibition in rat brain, which seems stronger with acute administration than chronic administration, while its mechanism remains to be further studied.

Objective To investigate the expression of hsa-miR-144 in esophageal squamous cell carcinoma, and its relationship with clinicopathological features and prognosis. Methods Reverse transcriptase polymerase chain reaction (RT-PCR) method was used to detect the hsa-miR-144 in 46 cases of esophageal squamous cell carcinoma and adjacent normal tissue. The expression of hsa-miR-144 in esophageal squamous cell carcinoma and its difference in the clinicopatho?logical characteristics including gender, age, and tumor size were investigated. The relationship between the expression of hsa-miR-144 and prognosis of patients with esophageal squamous cell carcinoma was analyzed. Kaplan-Meier method and Log-rank test were used to analyse the differences in survival rates in different pathological characteristics. Results The ex?pression level of hsa-miR-144 was lower in esophageal squamous cell carcinoma 0.97(0.22-24.48)×10-6 than that of adjacent normal tissue 8.60(0.09-258.20)×10-6, the difference was statistically significant (Z=2.221, P<0.05). The expression level of hsa-miR-144 was higher in esophageal squamous cell carcinoma with no lymph node metastasis than that in esophageal squa?mous cell carcinoma with lymph node metastasis (Z=2.758,P<0.05), and the expression level decreased with the increase in the pathological staging (Z=7.737,P<0.05). There were no significant differences in the expression levels of hsa-miR-144 between different gender, age, tumor size, tumor location, tumor differentiation and tumor invasion depth (all P>0.05). There was no correlation between the expression of hsa-miR-144 and prognosis in patients with esophageal squamous cell carcino?ma (rs=0.031, P=0.839). In the survival rate, there was no statistic significance between high expressive of hsa-miR-144 group and low expressive group (P=0.828). The survival rate was lower in patients with lymph node metastasis than that of pa?tients without lymph node metastasis. The survival rates were lower in patients with relatively deep invasion and higher patho?logic stage (P<0.05). Conclusion The expression of hsa-miR-144 is down regulated in esophageal squamous cell carcino?ma, and which is associated with lymph node metastasis and pathological staging of esophageal carcinoma. It shows that hsa-miR-144 may serve as an anti-oncogene in the occurrence and development of esophageal squamous cell carcinoma.

Objective: To study the effects of TCFC on proliferation and osteogenic action of osteoblast in neonatal rat calvaria cultures in vitro. Methods: Osteoblasts were isolated from neonatal rat calvaria through trypsin and collagenase digestion. The proliferation and collagen synthesis were assayed by 3H TdR and 3H proline incorporation. The activity of ALP was measured by p nitrophenyl sodium phosphate assay. The ipriflavone was used as positive control drug.Results: TCFC significantly promoted bone cell proliferation, alkaline phosphatase activity and collage synthesis.Conclusion: TCFC had the anti osteoporosis action by promoting osteoblast proliferation, ALP activity and collage synthesis.

Carcinoma, Squamous Cell ; metabolism ; mortality ; Esophageal Neoplasms ; metabolism ; mortality ; Humans ; MicroRNAs ; metabolism ; Prognosis

Objective To investigate the application prospective of carboxyfullerene C_3 as a radioprotectant or assistant for tumor radiotherapy.Methods Different concentrations of C_3 were incubated with K562 and AHH-1 cell,CCK-8 assay and trypan blue rejection test were performed to examine the influence of C_3 on the cell viability.Annexin V/PI staining and flow cytometry assay were applied to assess the cell cycle and apoptosis after 7-ray irradiation.Results C_3 showed little toxicity to AHH-1 cell with the survival rate over 95% ,but 600 mg/L of C_3 markedly inhibited the growth of K562 cell (82%) .Pretreatment of 100 mg/L C_3 significantly increased the survival rate of AHH-1 cell after 4 Gy irradiation compared with the single radiation group(71.3% vs 90.3%) ,but decreased the apoptosis rate (26.3% vs 12.6%) ,while the survival rate of K562 cell was decreased and the apoptosis rate was elevated with the increase of C_3 concentration.Moreover,the cell cycle analysis revealed the G_2 phase block in AHH-1 cell after radiation exposure was mitigated by C_3 pretreatment,but that in K562 cell was aggravated.Conclusions C_3 has good radioprotective effects on AHH-1 cells.For K562 cell,C_3 could inhibit the cell proliferation,promote the radiation induced apoptosis and aggravate the G_2 phase block.

Exposure of airborne particulate matter (PM) with an aerodynamic diameter less than 2.5 lm (PM2.5) is epidemiologically associated with lung dysfunction and respiratory symptoms, including pulmonary fibrosis. However, whether epigenetic mechanisms are involved in PM2.5-induced pulmonary fibrosis is currently poorly understood. Herein, using a PM2.5-induced pulmonary fibrosis mouse model, we found that PM2.5 exposure leads to aberrant mRNA 5-methylcytosine (m5C) gain and loss in fibrotic lung tissues. Moreover, we showed the m5C-mediated regulatory map of gene functions in pulmonary fibrosis after PM2.5 exposure. Several genes act as m5C gain-upregulated factors, probably critical for the development of PM2.5-induced fibrosis in mouse lungs. These genes, including Lcn2, Mmp9, Chi3l1, Adipoq, Atp5j2, Atp5l, Atpif1, Ndufb6, Fgr, Slc11a1, and Tyrobp, are highly related to oxidative stress response, inflammatory responses, and immune system processes. Our study illustrates the first epitranscrip-tomic RNA m5C profile in PM2.5-induced pulmonary fibrosis and will be valuable in identifying biomarkers for PM2.5 exposure-related lung pathogenesis with translational potential.

Objective:This study compares the magnetic resonance imaging (MRI) appearance of two types of breast tissue markers to investigate the appropriate clinical application of the markers.Methods:Breast MRI of 69 patients (78 masses) with breast tissue markers had been placed were analyzed retrospectively from November 2015 to August 2018 in our hospital. The sizes and shapes of breast tissue markers were assessed in axial fat-suppressed T2-weighted images, T1-weighted images and contrast-enhanced T1-weighed images.Results:The length of the coil nickel-free stainless steel markers were greater than ribbon titanium markers, with statistical difference in fat-suppressed T2-weighted images ( P=0.039). In contrast-enhanced T1-weighted images, all coil nickel-free stainless steel markers showed >6 mm diameter and round shape, and ribbon titanium markers showed >6 mm diameter ( n=20) or ≤6 mm diameter ( n=8), and round ( n=20), dot ( n=7) or band ( n=1) shapes. The categories of sizes and shapes in two types of breast tissue markers both had statistical significance ( P<0.001, P<0.001). Conclusions:Small breast lesions with breast tissue markers are not suitable for MRI evaluation. The artifact of ribbon titanium markers is smaller than coil nickel-free stainless steel markers, so they have less impact for lesions. The choice of the breast tissue markers and image evaluation methods should depend on the different clinical conditions.

Objective To predict and validate the core targets of Sijunzi Decoction through network pharmacology and animal experiments,and to explore the mechanism of action of Sijunzi Decoction in inhibiting the occurrence of adenomas in chronic colorectal inflammation.Methods Based on TCMSP,GeneCards and OMIM databases,screen potential targets for active components of Sijunzi Decoction and gene targets related to disease and immunity,construct a potential target regulatory network for active components of Sijunzi Decoction,analyze relevant pathways and core targets through pathway enrichment and protein interaction networks,and explore potential targets of Sijunzi Decoction in inhibiting intestinal diseases.By intervening in the DSS induced chronic colorectal inflammation mouse model with Sijunzi Decoction,the protective effect of Sijunzi Decoction on chronic colorectal inflammation mice was confirmed through changes in intestinal phenotype and pathological staining in each group of mice.Finally,the transcriptional levels and protein expression levels of the core targets related to Sijunzi Decoction predicted based on network pharmacology were verified through qRT PCR and Western Blot,further validating the mechanism of Sijunzi Decoction's inhibitory effect on the occurrence of adenomas in mice with chronic colorectal inflammation.Results Network pharmacology analysis shows that Sijunzi Decoction is related to inflammatory,immune,and tumor related pathways,and 15 related core targets have been screened and predicted.After intervention with Sijunzi Decoction in DSS chronic colorectal inflammation model mice,it slowed down the inflammatory response of the colon and significantly improved the number and size of intestinal tumors.QRT PCR and Western Blot further confirmed that the mechanism of action of Sijunzi Decoction is related to the core targets of network pharmacology prediction,EGFR,MAPK8,and CASP3.Conclusion Sijunzi Decoction can inhibit the expression levels of EGFR,MAPK8,and CASP3,exerting the effect of inhibiting the occurrence of adenomas in chronic colorectal inflammation.This provides a new idea for further exploring the mechanism of Sijunzi Decoction's inhibition of the occurrence of adenomas in chronic colitis.