To determine the protective effect of Chinese herbal medicine 814 on elastase-induced emphysema in hamsters.Animals were injected intratrachealy with elastase for emphysematous models, prophylactic-therapeutic groups were administrate with 814 through esophagus two weeks before the instillation of elastase untill animals were killed at three different time at first, second, and third month. Pulmonary artery pressure, blood gas analysis, heart index and the ratio of dried weight to wet weight of lungs (WW/DW) were examined. The lung paraffin sections were measured mean linear intercept (MLI), mean alveolar number (MAN), ratio of parenchyma area to total area (PA/TA) by the microscope-computer morphometric analysis system.WW/DW in the prophylactic-therapeutic groups was recovered at the same level with the controls, whereas the emphysematous were significantly increased (P < 0.05); and compared with the emphysematous groups, the prophylactictherapeutic groups significantly decreased in MLI, increased in MAN and PA/TA (P < 0.001 or P < 0.05).Administration of 814 could partly inhibit the development of emphysema induced by elestase in hamsters.
To observe preventive and therapeutic effect of Chinese herbs Naofeikang on hypoxic pulmonary artery hypertension of elastase-induced emphysema hamsters and investigate its mechanism.Hamsters for 30 days after intratracheally-instilled elastase, were kept in hypoxia environment under normal atmospheric pressure for 15 days, 50 hamsters were divided into prevention group (Prv), treatment group (T), emphysema + hypoxia (EH), and control group(N). Mean pulmonary artery pressure (MPAP) was measured before hamsters were killed. And then right ventricle hypertrophy index (RVHI) was measured, as well as circulating endothelial cells (CEC) and cells recoveries from bronchoalveolar lavage fluid (BALF) were counted. Meanwhile, pulmonary tissue changes were studied under light microscope with morphometric analysis.Compared with EH group, MPAP, CEC, and cells recoveries of BALF of Prv and T groups were significantly decreased (P < 0.05 or P < 0.01); Mean linear intercept and percentage of arterial media area of Prv and T groups had totally a significant difference (P < 0.01) in comparison with EH group.Chinese herbs Naofeikang could lower pulmonary hypertension, preserve vessel endothelial cells and lessen the inflammatory reaction in pulmonary tissue. Thereby, it could hinder the further development of emphysema and inhibit the remodeling of pulmonary small artery.
Background: To date no discrete genetic signature has been defined for isolated Dclk1+ tuft cells within the small intestine. Furthermore, recent reports on the functional significance of Dclk1+ cells in the small intestine have been inconsistent. These cells have been proposed to be fully differentiated cells, reserve stem cells, and tumor stem cells. Here we present a discrete candidate gene signature of Dclk1+ cells obtained from Dclk1-CreER;Rosa26-YFP mice, which will be a valuable animal model for future work seeking to uncover the latent abilities and functional role of Dclk1 expressing tuft cells and their subsets. Methods: The Dclk1-CreER;Rosa26-YFP compound mice were injected with tamoxifen to induce the expression of YFP driven by Dclk1 promoter. We FACS-sorted Dclk1+ cells from the small intestinal epithelium of Dclk1-CreER;Rosa26-YFP mice. We determined the mRNA expression levels of Dclk1 and other stem cell associated markers (Bmi1 and Lgr5), and pluripotency factors in the isolated Dclk1+ and Dclk1cells. To analyze the expression of key markers of quiescence survival and longevity, mRNA expression of cell cycle regulators and survival factors were analyzed. To explore the clonogenic capacity of the otherwise quiescent cells, we investigated self-renewal capacity in the Dclk1+ and Dclk1population. Results: Following tamoxifen administration, intestines were collected for YFP and Dclk1 staining, and we found that YFP co-localized with Dclk1 expression. Analysis of sorted YFP+ cells demonstrated marked enrichment (~6000 fold) for Dclk1 mRNA compared with YFPcells, confirming successful isolation of Dclk1+ cells. The Dclk1+ population was enriched (~6 fold) for the quiescent putative stem cell marker Bmi1, whereas the Dclk1fraction was enriched ~174 fold for Lgr5. We observed a relatively higher expression of pluripotency genes (~5-80 fold) as well as a significant increase in pro-survival genes (~4-9 fold) and quiescence regulatory markers (~8-24 fold) in the Dclk1+ cells compared to Dclk1cells. A 14-fold increase in self-renewal capability was observed in in vitro isolated Dclk1+ cells by clonogenic assay. The unique genetic profile presented in this study suggests that Dclk1+ cells may be relatively quiescent under normal homeostatic conditions but maintain their pluripotency and metabolic machinery required for survival/longevity through the expression of Cdkn1A, Cdkn1B, Oct4, Sox2, Nanog, and Klf4, Wif1, RelA, Akt and AMPK, and vital regulation of Raptor, Rictor, p53 and Survivin. Conclusion: Taken as a whole, these results provide additional support for the hypothesis that while the majority of Dclk1+ cells are committed tuft cells, they also maintain the molecular capability for stemness in reserve, and could play a role in the maintenance of the stem cell niche in an injury repair environment.
Ethyl pyruvate has been shown to ameliorate liver injury and decrease expression of several proinflammatory cytokines when used to treat mice with hemorrhagic shock or alcoholic hepatitis. Herein we sought to determine whether delayed treatment with ethyl pyruvate dissolved in a Ringer's-type balanced salt solution--Ringer's ethyl pyruvate solution (REPS)--would be beneficial in a murine model of common bile duct ligation (CBDL)-induced liver injury. Male C57BL/6 mice were subjected to a sham (n = 6) procedure or CBDL (n = 27). Twenty-four hours after operation, mice subjected to CBDL were randomized to receive treatment with either REPS (40 mg/kg of ethyl pyruvate per dose) or Ringer's lactate solution (RLS) every 8 h over a 72 h period. Compared with sham-treated controls, CBDL in RLS-treated mice was associated with histological evidence of hepatocellular necrosis as well as significant increases in the plasma concentrations of alanine aminotransferase and total bilirubin. Relative to sham-treated controls, CBDL in RLS-treated mice also was associated with increased hepatic lipid peroxidation and increased hepatic expression of transcripts for TNF, IL-6, and iNOS. All of these changes were significantly attenuated by delayed treatment with REPS after CBDL. In the RLS-treated group, CBDL was associated with increased NF-kappaB DNA binding in nuclear extracts prepared from liver tissue. Treatment with REPS increased NF-kappaB DNA binding still further. CBDL was associated with increased hepatocellular apoptosis in both the RLS- and REPS-treated groups. These data support the view that ethyl pyruvate ameliorates hepatic inflammation, lipid peroxidation, and necrosis in mice subjected to CBDL. Ethyl pyruvate warrants further evaluation as an adjunctive treatment to ameliorate liver injury from extrahepatic biliary obstruction.
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