ABSTRACT
To explore the protective effectof Likun preparation No.1 on bone marrow suppression injury in mice and the possible mechanism. Methods Sixty male BALB/c mice were randomly divided into normal control group, 5-Fu model group, positive control group(rhG-CSF) and Likun preparation No.1 groups with low, medium and high doses. Myocardial inhibition was established by intraperitoneal injection of 5-fluorouracil once. After seven days of administration, blood routine analysis was performed. Serum levels of TNF-α and IL-2 were detected by ELISA. The expression of p-JAK2 and p-STAT5 protein in spleen tissues were determined by Western blot. Results After given the Likun preparation No.1, the symptoms of diarrhea in mice were alleviated, body weight increased(P < 0.05), and white blood cells, platelets and lymphocytes also increased(P < 0.05). ELISA test showed that the serum level of IL-2 in Likun preparation high-dose group was higher than that in model group(P < 0.05), and the TNF-α content was lower than that in model group(P < 0.05). Western blot analysis showed that compared with model group, the expression of p-JAK2 and p-STAT5 protein in spleen of mice in Likun preparation group was up-regulated(P < 0.05). Conclusions The Likun preparation No.1 has protective effect on 5-Fu-induced myelosuppression in mice. The molecular mechanism may be related to the up-regulation of p-JAK2 and p-STAT5 protein expression, the promotion of IL-2 production and the reduction of TNF-α secretion.
ABSTRACT
Aim To explore the protective effects of naringin on hypoxic ischemic brain injury in neonatal rats and its mechanism. Methods Ninety-six healthy 7-day neonatal SD rats were randomly divided into sham operation group, hypoxic-ischemic brain damage group (HIBD group),HIBD with low-dose naringenin group(50 mg·kg-1, NG-L) and HIBD with high-dose naringenin group(100 mg·kg-1,NG-H). Neu-rological deficit, HE staining and brain water content were measured 48h after operation. Immunoblotting was used to detect the expressions of NOD2,RIP2 and NF-κB. Enzyme linked immunosorbent assay(ELISA) method was adopted to detect TNF-α and IL-1β ex-pression. Results Compared with HIBD group, the neurological deficit score decreased, the pathological damage was reduced, and the water content of brain tissues markedly decreased by naringenin(50,100 mg ·kg-1) treatment(P<0.05). Western blot revealed the down-regulation of NOD2,RIP2 and NF-κB by na-ringenin (50,100mg·kg-1) treatment (P<0.05). The content of TNF-α and IL-1β in brain tissues was lower than that of HIBD group (P <0.05). Conclu-sion Naringenin is likely to exert a protective role in neonatal rats of hypoxic ischemic brain injury perhaps through decreasing the expression of NOD2, RIP2 and NF-κB,and reducing the secretion of TNF-α and IL-1β.
ABSTRACT
<p><b>OBJECTIVE</b>To study the expression of enoyl CoA hydratase 1 (ECH1) and the effect when down-regulation of ECH1 gene expression in mouse hepatocarcinoma cell.</p><p><b>METHODS</b>Immunofluorescence was used for detecting the expression of ECH1, and stably transfected Hca-F cells with pGPU6/GFP/Neo-shRNA-ECH1 expression plasmids. Cell proliferation was assessed by Cell counting kit-8 (CCK8) assay. The Boyden-transwell assay (8 µm pore size) was performed to analyze the inhibitory effect of shRNA on Hca-F cell migration and invasion.</p><p><b>RESULTS</b>ECH1 expression was obtained in the cytoplasm and upregulated expression in Hca-F cells than that in Hca-P cells. The down-regulation of ECH1 could inhibit the cell proliferation of Hca-F cells, decrease the number of cell pass through Transwell (27.07 ± 17.49) compared with scramble-negative (72.38 ± 18.83) and Hca-F controls (59.06 ± 30.33), decrease the migration capacities of Hca-F cells, increase the ratio of Hca-F cells in S phase (86.1%) compared with scramble-negative (75.8%) and Hca-F controls (66.2%) and decrease the ratio of G(1) phase (9.4%) compared with scramble-negative (24.2%) and Hca-F controls (30.3%).</p><p><b>CONCLUSION</b>ECH1 serves as a potential critical factor attributes to tumor lymphatic metastasis.</p>