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Introduction: Low molecular weight heparin (LMWH), a natural sulfated glycosaminoglycan with an affinity for proangiogenic factors, is produced by chemical or enzymatic depolymerization of unfractionated heparin (UFH). Known for its anticoagulant effects, LMWH has recently been reported to have a strong anti-inflammatory effect on colitis, myocarditis, and airway inflammation. However, as a newly-developed drug, its anti-inflammatory mechanism in upper respiratory tract inflammation has not been well-studied. Methods: SD rats were randomly divided into control and experimental groups. The experimental group was established by building an acute nasal sinusitis model with expansion sponges mixed with Streptococcus pneumoniae . Then the experimental group rats were subcutaneously injected with different concentrations of LMWH. After seven consecutive days of injection, some rats were sacrificed, and blood and nasal mucosa samples were taken to determine their inflammation status. The remaining acute sinusitis rats were randomly selected for a week of nasal irrigation with normal saline or saline mixed with different concentrations of LMWH. One week later, rats were sacrificed, and samples of blood and nasal mucosa were taken to determine the inflammation status. Results: Rat nasal mucosa in the model group had obvious inflammation. The degree of nasal mucosa inflammation damage in the experimental group was lower than in the experimental control group, proving that LMWH has a protective effect on the nasal mucosa and that the effect correlates with dosage. Irrigation of the nose with saline mixed with LMWH can improve the anti-inflammatory effect. Protein related to the TLR4-MyD88-NF-κB signaling pathway was activated in the acute sinusitis rat model, and LMWH can significantly inhibit its expression. Conclusion: This is the first report of the anti-inflammatory effect of LMWH in acute upper respiratory tract inflammation, together with an explanation of its anti-inflammatory mechanism. The findings contribute a theoretical basis for its potential anti-tumor effect.

To investigate the anticancer effects of desacetyluvaricin (DES) on hepatocellular carcinoma (HCC) in vitro, and to study its mechanism. Using DES and cisplatin (DDP) to intervene the cell lines of hepatocarcinoma G2.2.15 (HepG2.2.15) and HepG2, by detecting the expression of HBxAg by immunofluorescence method, the cell cycle and apoptosis by flow cytometry method (FCM), and expression of NF-κB protein by ELISA. DES and DDP showed to suppress proliferation of HepG2.2.15 and HepG2; they increase the S-phase cells and decrease G2/M phase cells. DES and DDP both could promote the apoptosis and reduce the expression of NF-κB on the cell line. DES and DDP both can suppress the expression of HbxAg in HepG2.2.15. There were no statistical differences of the above results between these two drugs (P > 0.05). DES possesses anticancer effect on hepatocarcinoma. The possible mechanism might be due to promotion the apoptosis of the cancer cells, and downregulate the expression of HBx andNF-κB protein. DES is a kind of natural products, Because of the lighter clinical side effects; our observations suggest that DES has the potential to be explored as an effective anticancer agent for HCC.