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As the endogenous ligand for the GH secretagogue receptor (GHSR), Ghrelin is aberrant expressed in multiple malignant carcinoma, and involved in regulating a number of progression of cancer, especially in metastasis and proliferation. However, the precise role of Ghrelin in tumorigenesis of gastric cancer (GC) is still poorly understood. In this study, we extensively investigated the roles and mechanisms of Ghrelin in human gastric cancer. Ghrelin levels in cancer tissues and cell lines were analyzed by immunohistochemistry, qRT-PCR, and Western blot. Functional studies were performed after Ghrelin overexpressed or knockdown in AGS cell line. Cell proliferation was evaluated in by MTT and clone formation assays. The wound healing and Transwell system were used to assess the cell migration and invasive ability of GC cells. Cell apoptosis was detected by flow cytometry, and metabolic assays were performed to reveal the function of Warburg effect in the process. Ghrelin was lowly expressed in gastric cancer tissues and cell lines. Overexpression of Ghrelin inhibited gastric cancer cell proliferation, migration, invasion, and promoted apoptosis by activating the AMPK pathway, while D-[lys3]-GHRP-6 (a GHSR agonist) treatment relieved the effect, promoting tumorigenesis. Ghrelin knockdown increased the glucose uptake and lactic acid release, suggesting that Ghrelin elicited an anti-Warburg effect via AMPK pathway to inhibit gastric tumorigenesis. Ghrelin inhibits cell proliferation, migration, and invasion by eliciting an anti-Warburg effect via AMPK signaling pathway in gastric cancer cells.

Ghrelin is an orexigenic hormone that is produced by gastric cells. Ghrelin stimulates food intake and increases gastric movement. In rat model, injected β-hydroxybutyric acid (β-HB) leads to a decrease in body weight. It has been reported that patients with gastric erosions are slower to evacuate the stomach. The aim of the present study was to investigate the effects of ghrelin and β-HB on motility and inflammation in rat gastric antral smooth muscle cells (GASMCs). GASMCs were extracted from rat gastric antrum. Cell viability was determined using the Cell Counting Kit-8 assay. A reactive oxygen species (ROS) assay kit was used to analyze the levels of ROS using flow cytometry. Protein levels were determined using western blotting, and the expression levels of mRNAs were evaluated using reverse transcription-quantitative PCR. β-HB inhibited the expression of myosin regulatory light polypeptide 9 (MYL9), myosin light chain kinase (MLCK), transforming protein RhoA (RhoA), Rho-associated protein kinase-1 (ROCK-1) and growth hormone secretagogue receptor (GHS-R). By contrast, ghrelin increased the expression of MYL9, MLCK, RhoA, ROCK-1 and GHS-R in β-HB-treated GASMCs. β-HB increased the levels of tumor necrosis factor (TNF)-α, interleukin (IL)-6 and ROS, and decreased the levels of manganese (Mn) superoxide dismutase (SOD), copper/zinc (Cu/Zn)SOD and catalase. Ghrelin decreased the expression of TNF-α, IL-6, ROS and catalase, whereas ghrelin promoted the expression of MnSOD and Cu/ZnSOD in β-HB-treated GASMCs. Short interfering RNA targeting GHS-R inhibited the expression of MYL9, MLCK, RhoA and ROCK-1, and increased the levels of TNF-α, IL-6 and ROS in β-HB-treated or ghrelin-treated GASMCs. The present study provided preliminary evidence that β-HB inhibits the motility of GASMCs and promotes inflammation in GASMCs, whereas ghrelin decreases these effects. GHS-R acted as a primary regulator of motility and inflammation in GASMCs treated with β-HB and ghrelin.

To explore the effect of electroacupuncture（EA）on the expression of muscle-specific ring finger protein 1（MuRF1/Trim63），F-box only protein 32（Fbxo32），myosin heavy chain-IIa（Myh2），myosin heavy chain-IIb（Myh4）and myosin heavy chain-I（Myh7）in diabetes rats.Thirty-six male Wistar rats were equally randomized into control, model and EA groups. The diabetes model was established by intraperitoneal injection of 0.1% Streptozocin (STZ) solution (50 mg/kg). After that, EA (2 Hz, 1 mA) was applied to bilateral "Zusanli" (ST36), "Yinlingquan" (SP9) and "Shenshu" (BL23) for 10 min, once a day, 6 times a week for 2 weeks. The fasting blood glucose (FBG) and fasting serum insulin (FINS) contents were assayed by using ELISA, and the homeostasis model assessment of insulin resistance (HOMA-IR) was calculated. The body weight, and wet weight of bilateral gastrocnemius muscles were measured. The cross-sectional area (CSA) of the gastrocnemius muscle was measured after H.E. stai-ning. The expression of MuRF1, Fbxo32, Myh2, Myh4 and Myh7 mRNAs in the gastrocnemius tissue was tested using quantitative real time-PCR.Compared with the control group, the FBG and HOMA-IR were significantly higher (EA treatment can delay the atrophy of gastrocnemius muscle (skeletal muscle) in diabetes rats possibly by improving the degradation of myosin heavy chain via regulating the expression of muscular MuRF1, Fbxo32, Myh2, Myh4 and Myh7 mRNAs.

Excess fluoride intake could induce apoptosis in the cells. As an essential micronutrient and cytoprotectant, zinc is involved in many types of apoptosis. Here, we studied the effects of zinc and ZIP1 on fluoride-induced apoptosis in mouse MC3T3-E1 cells and examined the underlying molecular mechanisms. Our study found that fluoride not only inhibited cell proliferation and increased the intracellular reactive oxygen species (ROS) but also induced cell apoptosis. Whereas pretreatment with zinc significantly attenuated fluoride-induced ROS production and partly protected cells against fluoride-induced apoptosis through MAPK/ERK signaling pathway. Our study also found that fluoride upregulated the expression of ZIP1 in a time-dependent manner. Moreover, overexpression of ZIP1 also inhibited fluoride-induced apoptosis by activation of PI3K/Akt pathway. This cytoprotective effect of zinc and ZIP1 may be new factors that affect the physiological activity of fluoride and need study further.

Objective To describe the clinical characteristics and diagnostic features of giant lymph node hyperplasia or Castleman’s disease found in rare locations.

To investigate the inhibitory effect of danshensu on c-Jun N-terminal kinase (JNK) and nuclear factor-kappa B (NF-kappaB) signaling in activated rat hepatic stellate cells (HSCs) and explore the mechanisms of danshensu for inhibiting hepatic fibrosis.MTT colorimetric assay was used to detect the proliferation of rat HSCs treated with danshensu, and the apoptosis of the cells was analyzed with Annexin- V-FITC/PI and AO/EB staining. The expressions of P-IkappaB-alpha, NF-kappaBP65 and JNK in HSCs stimulated by IL-1beta with subsequent danshensu treatment were observed by Western blotting. Type III collagen in the medium of HSCs was detected by ELISA and immunocytochemistry.Danshensu inhibited the activation and proliferation of HSCs, and increased the apoptotic rate of HSCs and reduced the synthesis and secretion of type III collagen. Danshensu showed obvious inhibitory effect on JNK and P-IkappaB-alpha phosphorylation and NF-kappaBP65 expression in HSCs stimulated by IL-1beta. The mechanism of the actions of dansgensu may be mediated by inhibition of JNK and NF-kappaB signal transduction.

Drug resistant bacteria is an increasingly urgent challenge to public health. Bacteria adaptation and extensive abuse of antibiotics contribute to this dilemma. Active efflux of antibiotics is employed by the bacteria to survive the antibiotic pressure. Efflux pump is one of the hot spots of current drug related studies and ideal targets for the improvement of treatment. The efflux pumps and related mechanisms of action, regulation of expression and methodologies were summarized. Comparative genomics analyses were employed to elucidate the underlying mechanisms of action and evolution of efflux pump as exemplified by the Mycobacterium in our lab, which is a crucial re-emerging threat to global public health. The pathway and state-of-art drug development of efflux pump related drugs are included too.

To explore the correlation between the expressions of galectin-3 and E-cadherin and lymph node metastasis of colon cancer.Immunohistochemistry was employed to examine the expressions of E-cadherin and galectin-3 in 37 colon cancer samples, among which 21 samples underwent RT-PCR for E-cadherin and galectin-3 mRNA expressions. The correlation of E-cadherin and galectin-3 expressions with lymph node metastasis of the tumor was analyzed.The positivity rate of galectin-3 expression was 83.8% (31/37) in these samples. Of the tumor cases with lymph node metastasis, 94.7% (18/19) of the tumors were positive for galectin-3 expression, a rate significantly higher than that in non-metastatic cases. The positivity rate of E-cadherin expression was 59.5% (22/37) in the total cases, and 47.4% (9/19) in the metastatic cases, significantly lower than that in the non-metastatic cases.Galectin-3 and E-cadherin expressions are associated with lymph node metastasis of colon cancer and may serve as potential prognostic indicators for colon cancer patients.

Background The purpose of the present study was to examine the expression levels of microRNA-9 (miR-9) in osteosarcoma tissues and normal bone tissues, and investigate the relationships between miR-9 expression, clinicopathological features and the prognosis of patients with osteosarcoma. Methods The expression levels of miR-9 in osteosarcoma tissues and corresponding non-cancerous tissues were detected using a real-time quantitative assay. Differences in patient survival were determined using the Kaplan–Meier method and a log-rank test. A Cox proportional hazards regression analysis was used for univariate and multivariate analyses of prognostic values. Results Compared to non-cancerous bone tissues, the expression levels of miR-9 in osteosarcoma tissues were significantly elevated (P