Objective:To study the content determination method for the effective components in WudangⅡFlos lonicerae Caulis to lay foundation for the quality evaluation. Methods: An ultrasonic method was used. The effects of extraction solvent, ultrasonic time, ultrasonic power and ratio of solid to liquid on the contents of rutin and mignonette nucleoside were studied, and the extraction conditions were optimized by a 4-factor and 3-level orthogonal experiment. The chromatographic conditions were as follows:a Phenome-nex Luna-C18(250 mm ×4.60 mm, 5 μm) column was adopted for chlorogenic acid, and a Fortis Xi Phenyl column (250 mm × 4. 6 mm, 5 μm) was used for rutin, loganin and luteoloside;the mobile phase was acetonitrile (B)-0. 4% phosphoric acid (C) solu-tion (15 ∶85) for chlorogenic acid and loganin, and acetonitrile (B) -0. 5% glacial acetic acid aqueous solutjion (D) with gradient e-lution for rutin and luteoloside;the column temperature was 30℃, and the detection wavelength was 327,237,354 and 348 nm, re-spectively. Results:The optimum extraction conditions for rutin and luteoloside from WudangⅡFlos lonicerae Caulis were as follows:the extraction solvent was 60% ethanol, the solid-liquid ratio was 1 ∶30, the ultrasonic power and the ultrasonic time were 350 W and 50 min for rutin, and 250W and 60min for luteoloside. The content of chlorogenic acid, loganin, rutin and luteoloside was 10. 27, 6. 33, 0. 401 and 0. 450 mg·g-1 in the samples, respectively. Conclusion:The method is simple and convenient, accurate and re-producible, which can be used to control the quality of WudangⅡFlos lonicerae Caulis and provide reference for the further develop-ment.

This paper was to explore the effect of blood oxygen saturation (SO2) on oxidative damages of erythrocytes under the condition of oxidative stress. Keeping SO2 of cultured erythrocytes in vitro at the states of 0.3, 0.5, 0.7, 0.9 and 0.98, respectively, we induced oxidative stress by tert-buthylhydroperoxide (BHP, 0.15 mmol/L of final concentration). After incubation, antioxidant capacity was assessed by measuring content of reduced glutathin hormone (GSH) in erythrocytes. Methemoglobin (MetHb) content, lipid peroxidation (thiobarbituric acid-reactive substances, TBARS) and denatured globin-chains on the plasma membrane were measured to assess the extent of oxidative damages. The results showed that in the presence of BHP, GSH contents increased from 0.3 to 0.98 groups; MetHb, TBARS and globin-chains levels all dropped with the rise of SO2. In conclusion, antioxidant capacity and oxidative damages of erythrocytes are closely related to SO2, declined SO2 could promote oxidative damages of erythrocytes.
Cells, Cultured ; Erythrocytes ; cytology ; metabolism ; physiology ; Glutathione ; blood ; Humans ; Methemoglobin ; metabolism ; Oxidative Stress ; drug effects ; Oximetry ; methods ; Oxygen ; blood ; Thiobarbituric Acid Reactive Substances ; metabolism ; tert-Butylhydroperoxide ; toxicity

With the development of modern society, the incidence rate of cervicogenic headache (CEH) in the population is younger and increasing year by year. CEH is a common and unique form of headache, characterized by inflammation or physiological changes in cervical structures such as bones, intervertebral discs, or soft tissues, resulting in chronic, unilateral head pain as the main manifestation of the syndrome. The nature of pain often manifests as involving pain. The combination of traditional Chinese and western medicine in the treatment of CEH has gradually become a research hotspot in this field. This article reviews recent domestic and foreign literature on CEH and reviews the latest research progress of traditional Chinese and western medicine treatment in cervical headache.

Cancer-associated fibroblasts (CAFs) are one of the major cellularcomponents in tumor microenvironment (TME), which play an important role in cancer progression. MicroRNAs (miRNAs) could participate in the process of CAFs, transformation and metabolism reprogramming, affect the stemness of CAFs, and regulate CAFs-mediated tumor cell proliferation, invasion and chemotherapy resistance; and studies have shown that miRNAs play an important role in CAFs formation and the regulation of CAFs on tumors. The miRNAs released by CAFs can be used as reference indicators for tumor diagnosis, prognosis and drug selection. Thus, exploring the role of miRNAs in the interaction between CAFs and tumor cells and underlining the mechanism, is of great significancefor understanding the occurrence and development of tumors, as well as providing novel strategy for cancer treatment. This review will summarize the role of miRNAs in the formation of CAFs and the regulation of CAFs on tumor cells.

[Abstract] Objective: To investigate the molecular mechanism of microRNA-101 (miR-101) inhibiting the migration and invasion of non-small cell lung cancer (NSCLC) via targeting fibroblast growth factor 2 (FGF2). Methods: qPCR was used to detect the expression levels of miR-101 and FGF2 in human normal lung epithelial BEAS-2B cells and NSCLC cell lines (A549, H661 and SK-MES-1) as well as A549 cells after transfection. MiR-NC, miR-101 mimics, miR-IN-NC, miR-101 inhibitor or pcDNA-3.1 empty plasmid, pcDNA-FGF2 were respectively transfected into A549 cells. Wound healing assay and Transwell assay were used to examine the effects of overexpression of miR-101 and FGF2 on the migration and invasion of A549 cells. Western blotting(WB) was used to detect the expression levels of FGF2, E-cadherin, N-cadherin, Vimentin, ERK1/2 and p-ERK1/2 in A549 cells in each group. Results: The expression level of miR-101 in NSCLC cell lines were significantly lower than that in normal lung epithelial cells (all P<0.05), while the expression level in A549 cells was the lowest. Overexpression of miR-101 significantly inhibited the migration (P<0.05) and invasion (P<0.01) of A549 cells, increased the expression level of E-cadherin but decreased the expression level of Vimentin (P<0.05),N-cadherin (P<0.01) and p-ERK1/2 (P<0.05). Inhibition of miR-101 significantly enhanced the invasion and migration of A549 cells (all P<0.05), decreased the expression level of E-cadherin but increased the expression levels of Vimentin, N-cadherin and p-ERK1/2 (all P<0.05). The results of WB and Dual-luciferase reporter gene assay verified that FGF2 is a direct target gene of miR-101, and over‐expression of FGF2 significantly enhanced the invasion and migration of A549 cells (all P<0.01), decreased the expression of E-cadherin (P<0.01) but increased the expressions of Vimentin (P<0.01), N-cadherin (P<0.05) and p-ERK1/2 (P<0.01). Compared with the FGF2 overexpression alone group, co-overexpression of miR-101 and FGF2 significantly reduced the invasion and migration of A549 cells (all P<0.01), increased the expression of E-cadherin (P<0.01), and decreased the expressions of Vimentin (P<0.01), N-cadherin (P<0.05) and p-ERK1/2 (P<0.01). Conclusion: By targeting FGF2, miR-101 inhibits the invasion and migration of NSCLC cells through suppressing the epithelial-mesenchymal transition (EMT) and ERK signaling pathway.