ABSTRACT
As a member of the reticulin family, Nogo is mainly involved in processes such as tissue regeneration, apoptosis and tumor growth after tissue injury. Cardiovascular disease is one of the main diseases that threaten human health at present. In recent years, research on Nogo in the cardiovascular system has become increasingly extensive. Changes in the expression of Nogo during myocardial fibrosis, myocardial cell apoptosis and vascular remodeling suggest that it may play a certain role. This article reviews the distribution of Nogo in the heart and its role in cardiovascular disease, in order to reveal its possible role and mechanism in cardiovascular diseases.
ABSTRACT
Objective To investigate the change of disease constitution at different stages of a long voyage on the sea in a frigate. Methods The participants included the crew members in a frigate of PLA navy force. The disease types of the crew members were recorded at different stages of a long voyage on the sea in the frigate, including the whole voyage, early stage of voyage, middle stage of voyage and the late stage of voyage. Then, the disease constitution ratios at different stages was calculated, compared and sorted. Results It was found that the disease constituent ratios during the whole course, from high to low, was: respiratory infection,acute gastroenteritis,lumbar muscle degeneration,insomnia,kinetosis,dermatitis,oral ulcer,conjunctivitis,trauma,disease of cardiovascular system,paronychia and urinary calculi. The ranking during the early stage, from high to low, was: kinetosis, respiratory infection,trauma,acute gastroenteritis,lumbar muscle degeneration,disease of cardiovascular system,insomnia and dermatitis; the ranking during the middle stage was respiratory infection,acute gastroenteritis,lumbar muscle degeneration,insomnia,dermatitis,oral ulcer,trauma,conjunctivitis, urinary calculi and paronychia; and that during the late stage was: respiratory infection,lumbar muscle degeneration,insomnia,dermatitis,oral ulcer,acute gastroenteritis,conjunctivitis,kinetosis,disease of cardiovascular system,trauma,urinary calculi and paronychia. Conclusion Both the disease type and the disease constitution of the crew members change during different stages of a long voyage on the sea in a frigate.
ABSTRACT
Objective: To observe the effect of andrographolide on the expression of TNF-α and IL-12 in activated macrophages. Methods: The peritoneal macrophages were harvested from mice intraperitoneally injected with thioglycollate. The macrophages were pretreated with andrographolide and then stimulated with lipopolysaccharide. RT-PCR was used to examine the expression of TNF-α, IL-12a, and IL-12b in the macrophages, and ELISA was used to measure the protein levels of TNF-α and IL-12 in the supernatant. Results: Andrographolide inhibited the mRNA levels of TNF-α, IL-12a, and IL-12b, and the protein levels of TNF-α and IL-12 in activated macrophages, and the inhibition increased with the increase of andrographolide concentration. Andrographolide at 12 μg/ml (P<0.05) and 25 μg/ml (P<0.01) significantly inhibited TNF-α mRNA level in macrophages; andrographolide at 1 μg/ml (P<0.05) and 12 μg/ml (P< 0.01) significantly inhibited TNF-α protein level (P<0.01). Andrographolide at 1 μg/ml significantly inhibited IL-12b mRNA level and at 12 μg/ml significantly inhibited IL-12a mRNA level (P<0.01); and andrographolide at 1 μg/ml also significantly inhibited IL-12 protein level (P<0.01). Conclusion: Andrographolide can inhibit both the expression of TNF-α and IL-12 in activated macrophages.
ABSTRACT
Objective: To establish a mouse hepatocellular carcinoma cell line that can produce mMIP-1α and to evaluate the possibility of cancer gene therapy by mMIP-1α. Methods: mMIP-1α cDNA was cloned into retrovirus vector pBabe puro and pBabe puro-mMIP-1α was constructed, then pBabe puro-mMIP-1α was used to transfect packaging cells, anti-puromycin cells was proliferated, the supernatant was used to infect hepa1-6, the anti-puromycin clone (hepa1-6 mMIP-1α) and hepa1-6 were analysed for the expression of mMIP-1α mRNA and protein by RT-PCR and immunohistochemistry respectively. The growth curve of hepa1-6 and hepa1-6 mMIP-1α was drawn. The chemotaxis of mMIP-1α produced by hepa1-6 mMIP-1α to mouse spleen cells was observed on agarose gel. C57B/L mouse was inoculated with the tumor cell and the tumorigenicity was studied. Results: Recombinant retrovirus vector pBabe puro-mMIP-1α with mMIP-1α cDNA was constructed. Hepa1-6 did not produce mMIP-1α mRNA and protein, while hepa1-6 mMIP-1α could produce mMIP-1α mRNA and protein. The growth curve of hepa1-6 and hepa1-6 mMIP-1α showed no difference. The chemotaxis of mMIP-1α produced by hepa1-6 mMIP-1α to mouse spleen cells was observed. The tumorigenicity was reduced. Conclusion: A mouse hepatocellular carcinoma Hepa1-6 mMIP-1α is established and mMIP-1α can affect the tumorigenecity of hepa1-6.
ABSTRACT
Objective: To establish a mouse hepatocellular carcinoma cell line that can produce mMIP-1α and to evaluate the possibility of cancer gene therapy by mMIP-1α. Methods: mMIP-1α cDNA was cloned into retrovirus vector pBabe puro and pBabe puro-mMIP-1α was constructed, then pBabe puro-mMIP-1α was used to transfect packaging cells, anti-puromycin cells was proliferated, the supernatant was used to infect hepa1-6, the anti-puromycin clone (hepa1-6 mMIP-1α) and hepa1-6 were analysed for the expression of mMIP-1α mRNA and protein by RT-PCR and immunohistochemistry respectively. The growth curve of hepa1-6 and hepa1-6 mMIP-1α was drawn. The chemotaxis of mMIP-1α produced by hepa1-6 mMIP-1α to mouse spleen cells was observed on agarose gel. C57B/L mouse was inoculated with the tumor cell and the tumorigenicity was studied. Results: Recombinant retrovirus vector pBabe puro-mMIP-1α with mMIP-1α cDNA was constructed. Hepa1-6 did not produce mMIP-1α mRNA and protein, while hepa1-6 mMIP-1α could produce mMIP-1α mRNA and protein. The growth curve of hepa1-6 and hepa1-6 mMIP-1α showed no difference. The chemotaxis of mMIP-1α produced by hepa1-6 mMIP-1α to mouse spleen cells was observed. The tumorigenicity was reduced. Conclusion: A mouse hepatocellular carcinoma Hepa1-6 mMIP-1α is established and mMIP-1α can affect the tumorigenecity of hepa1-6.