PubMed Health⌕ Search

Biomedical subjects

Nan Dong

Publications and source records attributed to Nan Dong.

5 recordsLinked to original sources
PubMed2006

[Research progress in Laggera medicinal plants].

This paper reviewed the worldwide research progresses of the genus Laggera both on phytochemical and pharmacological work in the past few decades. The main secondary metabolites of this genus are proved to be sesquitepenoids, flavonoids and phenolic acids. Phamacological investigations revealed that the certain extracts of some Laggera species possess significant bioactivities on anti-inflammation, anti-tumor and anti-viral infection. This review afforded the comprehensive description of the active components as to provide useful references to elucidate their historical clinical application on upper respiratory infection, influenza, parotitis, and recurrent herpes viral infection.

Animals↗
PubMed2005

Hepatitis B virus X protein upregulates survivin expression in hepatoma tissues.

The hepatitis B virus X protein (HBx) plays an important role in the development of hepatocellular carcinoma (HCC). The relationship was examined between HBV antigens and IAP (inhibitor of apoptosis) family in development of HCC. The expression levels of HBV antigens (HBsAg, HBcAg, and HBxAg) and members of the IAP family (survivin, XIAP, cIAP-1, and cIAP-2) were detected immunohistochemically in tissues from 34 cases of HCC and 30 cases of liver cirrhosis. The positive rate of survivin was higher than these three molecules in all three tissue types (P < 0.05). The positive rates of HBxAg and survivin were high in HCC (76.5% and 88.2%), paratumor (85.3% and 91.2%), and liver cirrhosis (100% and 93.3%) tissues, with no significant differences between the survivin- and HBxAg-positive rates (each P > 0.05). To examine the effect of HBx on survivin expression, plasmid pCMV-X (encoding the HBx gene) was transfected transiently with or without plasmid pcDNA3-sur (encoding the survivin gene) into H7402 hepatoma cells and L-O2 human normal liver cells. Cells over-expressing HBx alone showed increased apoptosis along with a dose-dependent increase in survivin levels. However, co-expression of survivin inhibited the HBx-induced apoptosis. To examine the effect of HBx on survivin in hepatoma cells without apoptosis, plasmid pCMV-X was transfected stably into human hepatoma H7402 cells and L-O2 cells. These H7402-X and L-O2-X cells showed high-level expression of both HBx and survivin, but did not show apoptosis. The addition of pSilencer 3.0-X, an RNAi vector targeting the HBx gene, reduced the expression levels of survivin protein in H7402-X cells. Collectively, these data demonstrate that HBx upregulates survivin expression in hepatoma tissues, suggesting that HBx and survivin may both be involved in carcinogenesis of HCC.

Adult↗
PubMed2005

Effects of hepatitis B virus X protein on human telomerase reverse transcriptase expression and activity in hepatoma cells.

In subjects with hepatitis B, carcinogenesis has been associated with the hepatitis B virus (HBV) X protein (HBX) and human telomerase reverse transcriptase (hTERT). In the experiments reported here, we used immunohistochemical methods to study the expression of hTERT and HBV antigens (HBsAg, HBcAg and HBxAg) in 34 cases of HCC and corresponding paratumor tissues, 30 cases of liver cirrhosis, and 6 normal livers. To examine the effect of HBX on hTERT expression and activity in hepatoma cells, we transiently and stably transfected the pCMV-X plasmid cloned HBx gene into H7402 hepatoma cells, then measured the expression of c-Myc and hTERT in these cells with the use of Western-blot analysis. Telomerase activity was detected with the use of the telomerase repeat amplification protocol (TRAP) in transiently and stably transfected cells. We found that hTERT expression was 67.6%, 73.5%, and 100% in tumor, paratumor, and cirrhosis samples, respectively, but found no hTERT positivity in samples of normal liver. HBsAg, HBcAg, and HBxAg were expressed in 58.8%, 26.5%, and 76.5% of tumor tissues, respectively; in 64.7%, 41.2%, and 85.3% of the corresponding paratumor tissues; and in 76.7%, 66.7%, and 100% of cirrhotic tissues. The chi 2 test revealed no significant difference between the expression of hTERT and HBxAg in these tissues. Western-blot analysis revealed that expression of c-Myc and hTERT in the transiently transfected cells was much greater than that in the control cells. We elicited a similar result when we used the TRAP method to measure telomerase activity. Our data collectively demonstrate that HBX up-regulates the expression and activity of hTERT in hepatoma cells, suggesting that hTERT is associated with tumor development.

Adult↗
PubMed2002

[Expression of mitogen-activated protein kinase and its upstream regulated signal in human hepatocellular carcinoma].

OBJECTIVE: To detect protein expression of ERK(1), ERK(2), JNK(1), p38 and MEK(1), MEK(2) in human hepatocellular carcinoma and adjacent non-neoplastic liver. METHODS: In 16 surgically resected hepatocellular carcinoma and para-carcinoma tissues, Western blotting was used to detect expression of ERK(1), ERK(2), JNK(1), p38 and MEK(1), MEK(2). RESULTS: In all cases, ERK(1), ERK(2), p38 expression in hepatocellular carcinoma was significantly higher than that in para-carcinoma: integral optic density (IOD) of ERK(1) was 300 +/- 98 in carcinoma and 98 +/- 48 in para-carcinoma tissues (t = 2.519, P < 0.01); IOD of ERK(2) was 587 +/- 83 in carcinoma and 232 +/- 96 in para-carcinoma tissues (t = 2.745, P < 0.01); IOD of p38 was 270 +/- 85 in carcinoma and 107 +/- 88 in para-carcinoma tissues (t = 2.491, P < 0.01). JNK(1) expression in hepatocellular carcinoma was significantly lower than that in para-carcinoma; IOD of JNK(1) was 111 +/- 93 in carcinoma and 292 +/- 109 in para-carcinoma tissues (t = 2.473, P < 0.01). Protein levels of MEK(1) and MEK(2) in carcinoma were significantly higher than in para-carcinoma. IOD of MEK(1) was 1 418 +/- 244 in carcinoma and 806 +/- 90 in para-carcinoma tissues (t = 2.546, P < 0.01). IOD of MEK(2) was 1 041 +/- 122 in carcinoma and 468 +/- 40 in para-carcinoma tissues (t = 2.861, P < 0.01). CONCLUSIONS: ERK(1), ERK(2), MEK(1) and MEK(2) in the signal transduction pathway for cell proliferation are significantly overexpressed and the expression of JNK(1) is lower in hepatocellular carcinoma. Their unbalance is one of the important reasons for the over growth and infinite proliferation of the hepatocellular carcinoma cell. The p38 and JNK(1) may be activated by different pathway.

Adult↗