[Effects of target tree management of Pinus massoniana plantation on soil nematode community structure at different soil depths]. / ç›®æ ‡æ ‘ç»è¥å¯¹é©¬å°¾æ¾äººå·¥æž—ä¸åŒåœŸå±‚æ·±åº¦åœŸå£¤çº¿è™«ç¾¤è½ç»“æž„çš„å½±å“.

To understand soil nematode community structure at different soil depths and its responses to target tree management, we collected soil samples (0-10, 10-20, and 20-50 cm) and litter samples from the target tree management plots and control plots of Pinus massoniana plantation and analyzed community structure, soil environmental factors, and their relationship. The results showed that target tree management increased the abundance of soil nematodes, with the most significant effect at a depth of 0-10 cm. The highest abundance of herbivores was found in the target tree management treatment, while that of bacterivores was found in the control. Compared with the control, Shannon diversity index, richness index, maturity index of nematodes at 10-20 cm soil layer and Shannon diversity index at 20-50 cm soil layer of target trees were significantly improved. According to the results of Pearson correlation and redundancy analysis, soil pH, total phosphorus, available phosphorus, total potassium, and available potassium were the main environmental factors affecting community structure and composition of soil nematodes. In general, target tree management was conducive to the survival and development of soil nematodes and promoted the sustainable development of P. massoniana plantations.

[Chrysin inhibited epithelial-mesenchymal transition of type â ¡ alveolar epithelial cell by regulating NF-κB/Twist 1 signaling pathway].

This study aimed to assess whether chrysin(ChR) can inhibit epithelial-mesenchymal transition(EMT) of type Ⅱ alveolar epithelial cell and produce anti-pulmonary fibrosis effect by regulating the NF-κB/Twist 1 signaling pathway. Sixty rats were randomly divided into the control group, the bleomycin(BLC) group, BLC+ChR(50 mg·kg~(-1)) group and BLC+ChR(100 mg·kg~(-1)) group, with 15 rats in each group. The pulmonary fibrosis model was induced by intratracheal injection of BLC(7 500 U·kg~(-1)). Rats were orally administered with different doses of ChR after BLC injection for 28 days. The cells were divided into control group, TGF-ß1 group(5 ng·mL~(-1)), and TGF-ß1+ChR(1, 10, 100 µmol·L~(-1)) groups. The type Ⅱ alveolar epithelial cells were treated with TGF-ß1 for 24 h, and then treated with TGF-ß1 for 48 h in the presence or absence of different doses of ChR(1, 10 and 100 µmol·L~(-1)). The morphological changes and collagen deposition in lung tissues were analyzed by HE staining, Masson staining and immunohistochemistry. The mRNA and protein expression levels of collagen Ⅰ, E-cadherin, zonula occludens-1(ZO-1), vimentin, alpha smooth muscle actin(α-SMA), inhibitor of nuclear factor kappa B alpha(IκBα), nuclear factor-kappa B p65(NF-κB p65), phospho-NF-κB p65(p-p65) and Twist 1 in lung tissues and cells were detected by qPCR and Western blot, respectively. The animal experiment results showed that as compared with the BLC group, after administration of ChR for 28 days, bleomycin-induced pulmonary fibrosis in rats was significantly relieved, collagen Ⅰ expression in lung tissues was significantly reduced(P<0.05 or P<0.01), and EMT of alveolar epithelial cells was obviously inhibited [the expression levels of E-cadherin and ZO-1 were increased and the expression levels of vimentin and α-SMA were decreased(P<0.05 or P<0.01)], concomitantly with significantly reduced IκBα and p65 phosphorylation level in cytoplasm and decreased NF-κB p65 and Twist 1 expression in nucleus(P<0.05 or P<0.01). The cell experiment results showed that different doses of ChR(1, 10 and 100 µmol·L~(-1)) significantly reduced TGF-ß1-induced collagen Ⅰ expression(P<0.05 or P<0.01), significantly inhibited EMT of type Ⅱ alveolar epithelial cells[the expression levels of E-cadherin and ZO-1 were increased and the expression levels of vimentin and α-SMA were decreased(P<0.05 or P<0.01)], and inhibited IκBα and p65 phosphorylation in cytoplasm and down-regulated NF-κB p65 and Twist 1 expression in nucleus induced by TGF-ß1(P<0.05 or P<0.01). The results suggest that ChR can reverse EMT of type Ⅱ alveolar epithelial cell and alleviate pulmonary fibrosis in rats, and its mechanism may be associated with reducing IκBα phosphorylation and inhibiting NF-κB p65 phosphorylation and nuclear transfer, thus down-regulating Twist 1 expression.

[Effects of thinning intensity on species composition and diversity of undergrowth vegetation community in Pinus massoniana plantation at initial stage of thinning]. / é—´ä¼å¼ºåº¦å¯¹é©¬å°¾æ¾äººå·¥æž—é—´ä¼åˆæœŸæž—ä¸‹æ¤è¢«ç¾¤è½ç‰©ç§ç»„æˆå’Œå¤šæ ·æ€§çš„å½±å“.

Species composition and diversity of undergrowth vegetation community under different thinning intensities (0, 10%, 20%, 30%, 40%, 50%) were examined at the initial stage of thinning in 29-year-old Pinus massoniana plantation in the low mountain region of eastern Sichuan. The results show that all the thinning treatments could reduce the absolute dominance of Miscanthus sinensis and Dicranopteris dichotoma. The dominant species composition of shrubs in each treatment was different. There were more extensive species in the medium thinning intensity (20%, 30% and 40%) treatments than other treatments. The diversity indices increased first and then decreased with increasing thinning intensity. The variation degree of herbs was stronger than shrubs. The diversity indices of herbs were positively correlated with soil water content. The explanation amount of thinning intensity and soil physicochemical properties to community differentiation was 81%. The vegetation communities in the medium thinning intensity forests showed positive correlation with all the factors except total phosphorus. At the initial stage of thinning, herbaceous communities were more sensitive to disturbance than shrub communities. The 40% thinning intensity treatment was more closely related to soil environmental factors, with high stability and the most abundant species, which would be the best thinning measure under the experimental condition.

[Rutaecarpine protects against bleomycin-induced pulmonary fibrosis through inhibiting Notch1/eIF3a signaling pathway in rats].

To investigate whether the protection of rutaecarpine against bleomycin-induced pulmonary fibrosis is mediated by inhibiting Notch1/eukaryotic initiation factor 3a (eIF3a) signaling pathway, and whether these effects are related to the synthesis and release of calcitonin gene-related peptide (CGRP) and inhibition of epithelial-mesenchymal transition (EMT) of alveolar epithelial cells, male Sprague-Dawley rats were randomly divided into five groups (n=12), respectively, Control group, bleomycin group, rutaecarpine (100, 300 mg·kg⁻¹) group and capsaicin plus rutaecarpine (300 mg·kg⁻¹) group. Bleomycin (5 mg·kg⁻¹) was used to induce pulmonary fibrosis rat model. Rats were given capsaicin (50 mg·kg⁻¹) by subcutaneous injections 1 days before and 7, 14, 21 days after induce pulmonary fibrosis rat model to deplete endogenous CGRP. At the end of experiments, blood was collected from carotid artery to determinate the plasma levels of CGRP by ELISA. Pulmonary tissue change was observed by HE staining. Masson's trichrome stain was used to demonstration collagen deposition. The collagen I expression in pulmonary tissue was measured by immunohistochemisty. The expression of CGRP, Notch1, eIF3a, collagen I, vimentin, alpha-smooth muscle actin (α-SMA), E-cadherin and zonula occludens-1 (ZO-1) was detected by qPCR or Western blot. Compared with the control group, the pulmonary tissue of the bleomycin group showed significant fibrosis, including significant disturbed alveolar structure, marked thickening of the interalveolar septa and dense interstitial infiltration by inflammatory cells and fibroblasts, and concomitantly with the decrease in plasma CGRP and expression of CGRP. Importantly the expression of E-cadherin and ZO-1 was decreased and expression of Notch1, eIF3a, collagen I, vimentin and α-SMA was increased in bleomycin group (P<0.05 or P<0.01). Compared with the bleomycin group, rutaecarpine (100, 300 mg·kg⁻¹) group significantly reduced bleomycin-induced pulmonary injury concomitantly with the increase in plasma CGRP and expression of CGRP. Importantly the expression of E-cadherin and ZO-1 was increased and expression of Notch1, eIF3a, collagen I, vimentin and α-SMA was decreased by rutaecarpine treatment (P<0.05 or P<0.01). All these effects of rutaecarpine were abolished by capsaicin.These results suggest that rutaecarpine protects against bleomycin-induced pulmonary fibrosis by inhibiting Notch1/eIF3a signaling pathway, alleviating EMT process, which is related to the increased synthesis and release of CGRP.

[Effect of sesamin on pulmonary vascular remodeling in rats with monocrotaline-induced pulmonary hypertension].

OBJECTIVE: To observe the effect of sesamin (Ses) on pulmonary vascular remodeling in rats with monocrotaline ( MCT)-induced pulmonary hypertension (PH). METHOD: Totally 48 male Sprague-Dawley (SD) rats were fed adaptively for one week and then divided into the normal control group, the MCT group, the MCT +Ses (50 mg x kg(-1)) group and the MCT + Ses (100 mg x kg(-1)) group, with 12 rats in each group. The PH rat model was induced through the subcutaneous injection with MCT(60 mg x kg(-1)). After the administration for four weeks, efforts were made to measure the right ventricular systolic pressure( RVSP) and mean pulmonary artery pressure (mPAP) through right jugular vein catheterization, and isolate right ventricle( RV) and left ventricle( LV) +septum (S) and measure their length to calculate RV/ ( LV + S) and ratio of RV to tibial length. Pathologic changes in arterioles were observed by HE staining. Masson's trichrome stain was used to demonstrate changes in collagen deposition of arterioles. The alpha-smooth muscle actin (alpha-SMA) expression in pulmonary arteries was measured by immunohistochemisty. The total antioxidative capacity (T-AOC) and malondialdehyde (MDA) content in pulmonary arteries were determined by the colorimetric method. The protein expressions of collagen I, NOX2 and NOX4 were analyzed by Real-time PCR and Western blot. RESULT: After the administration for 4 weeks, Ses could attenuate RVSP and mPAP induced by MCT, RV/ (LV + S) and ratio of RV to Tibial length, alpha-SMA and collagen I expressions and remodeling of pulmonary vessels and right ventricle. Meanwhile, Ses could obviously inhibit the expressions of NOX2, NOX4 and MDA content and increase T-AOC. CONCLUSION: Sesamin could ameliorate pulmonary vascular remodeling induced by monocrotaline in PH rats. Its mechanism may be related to expressions of NOX2 and NOX4 expression and reduction in oxidative stress injury.