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Objective: To observe the effects of curcumin on pulmonary fibrosis and functions on paraquat (PQ)-challenged rats, and investigate the possible mechanism., Methods: 108 SPF Wistar rats were divided into three groups according to random number sheet: normal saline (NS) control group, PQ model group and curcumin-treatment group. The rats in each group were subdivided into three subgroups according to different time points (3, 7, 14 days), with 12 rats in each subgroup. PQ-challenged models were reproduced by intragastrical administration of PQ solution 50 mg/kg, and those in NS control group were given the equal volume of NS. After 30 minutes, the rats in curcumin-treatment group were given 200 mg/kg of curcumin by intraperitoneal injection, and those in NS control group and PQ model group were given the equal volume of NS. At 3, 7, 14 days, the tidal volume (VT) was examined, and the blood was drawn from femoral artery for blood gas analysis. Then the rats were sacrificed and the lung tissues were harvested, the hydroxyproline (Hyp) content was measured by alkaline hydrolysis; the expression of transforming growth factor-β1 (TGF-β1) was determined by immuno-histochemistry; the distribution and the change of the pulmonary collagen fiber were observed after Masson staining., Results: After exposure to PQ, the VT and arterial partial pressure of oxygen (PaO 2 ) were decreased gradually, and the levels of Hyp and TGF-β1 were increased gradually, reaching the trough or the peak at 14 days, which were significantly lower or higher than those in NS control group [14-day VT (mL): 1.52±0.33 vs. 2.81±0.47, 14-day PaO 2 (kPa): 5.87±0.95 vs. 14.15±1.02, 14-day Hyp (μg/mg): 3.12±0.06 vs. 1.14±0.05, 14-day TGF-β1 (integral A value): 29.72±4.27 vs. 4.15±0.52, all P < 0.01]. After intervene of curcumin, the parameters were significantly improved as compared with those of PQ model group [14-day VT (mL): 2.34±0.19 vs. 1.52±0.33, 14-day PaO 2 (kPa): 10.23±1.01 vs. 5.87±0.95, 14-day Hyp (μg/mg): 2.31±0.04 vs. 3.12±0.06, 14-day TGF-β1 (integral A value): 15.46±2.89 vs. 29.72±4.27, all P < 0.01]. It was shown by Masson staining that in PQ model group, with the PQ-poisoned time prolonging, diffused pulmonary fibrosis and a large number of collagen deposition were observed gradually, and the most serious collagen deposition was observed at 14 days; after intervene of curcumin, pulmonary fibrosis was alleviated significantly at different time points as compared with the PQ model group., Conclusions: Curcumin can enhance the pulmonary function by reducing the deposition of collagen fiber and inhabiting pulmonary fibrosis of PQ-poisoned rats.

As a renewable energy sources to replace conventional fossil fuels, biodiesel fuels have been becoming increasingly requirements to global fuels market. Biodiesel derived from oil crops cannot realistically satisfy even more fraction of the raw material existing costs and soil competitive demand for its growth. Microalgae appear to be the advantage of costs that is capable of higher photosynthetic efficiency, larger biomass, faster growth compared to those of oil crops. Lipid content of many microalgae is usually 80% of its dry weight. Genetic microalgae with high-oil productivity by genetic manipulations are capable of making microalgal biodiesel economically competitive with petrodiesel through large-scale production of genetic microalgal biomass. As demonstrated here, the use of biodiesel fuels in home and abroad are currently introduced, and the cost advantage of microalgae as the raw material is analyzed; And moreover, the progress of microalgal genetic engineering in regulation of lipid metabolism and the problems in the construct of genetic microalgae strains as well as approaches for making microalgal biodiesel appear to be an important source of renewable fuel that has the potential to completely displace fossil diesel are discussed in this review.

In order to unveil the anti-angiogenic mechanism of triptolide, we investigated the effects of triptolide on the proliferation, migration, angiogenesis and u-PA expression of cultured HUVECs. MTT assay found that triptolide could inhibit the proliferation of HUVECs, and three-dimensional culture system revealed that triptolide could curb the migration of HUVECs. The chick embryo chorioallantoic membrane (CAM) test showed that triptolide could inhibit angiogenesis. Real time quantitive RT-PCR showed the expression of u-PA of HUVECs was down-regulated by triptolide. Therefore, triptolide may inhibit the proliferation and migration of endothelial cell by way of reducing the expression of u-PA. These findings may conduce to the elucidation of the anti-angiogenic mechanism of triptolide.