Fiber Septa Research Articles

Trabeculae and Al-accumulation in the wood cells of Melastomataceae species from Brazilian savanna

Family Melastomataceae is an important component of the Brazilian Cerrado flora, inhabiting different environments from those with well-drained soils to swamp soil sites. Several members of this family are recognized as aluminum (Al)-accumulating. We studied the wood anatomy of six species of Melastomataceae (Miconia albicans (Sw.) Triana, M. fallax DC., M. chamissois Naudin, M. ligustroides (DC.) Naudin, Microlepis oleaefolia (DC.) Triana, Rhynchanthera dichotoma DC.), growing in different environments of Cerrado, exploring the occurrence of trabeculae and Al-accumulation sites. We processed the material following the usual techniques in wood anatomy and histochemistry. We used a chrome azurol-S spot-test in fresh material to detect Al-accumulation. The common features were diffuse porosity, vessel elements with simple perforation plates and vestured pits, abundant parenchyma-like fiber bands and septate fibers, axial parenchyma scanty to vasicentric, and heterocellular rays. The presence of trabeculae in vessel elements, septa in parenchyma cells, and aluminum in the G-layer of the gelatinous fiber walls, in the septa of fibers, in cambial initials and derivatives cell walls, and in the vacuole of ray cells are recorded for the first time for Melastomataceae. The results of this study indicate an additional role for gelatinous fibers in Al-accumulation, and offer a new perspective on Al-compartmentalization in the wood cells from Cerrado species.

Experimental research on anti-fibrosis effect of Fuzheng-Liqi mixture in rat hepatic fobrosis induced by alcohol

Objective To explore the mechanisms and preventive effects of Fuzheng-Liqi mixture on alcoholic hepatic fibrosis. Methods 48 male SD rats were randomly divided into four groups: normal group, model group, Compound Salviae Miltiorrhizae (CSM) group and Fuzheng-Liqi mixture (FLM) group. Alcohol was poured into stomach of the rats for 16 weeks to induce hepatic fibrosis. At the same time, CSM and FLM were given to each group. The rats were killed after 16 weeks. Histomorphylogic structure of the liver tissues was observed under optical microscope; the levels of MDA and SOD in rounded by thick cords of collagen fibers, which extended from the portal areas and central veins. Obvious cloudy swelling could be seen in hepatocytes. Fatty degeneration was extensive, and some with necroses fiber septa were infiltrated by a great number of cells such as monocytes, lymphocytes, eosinophilic granulocytes, fibroblasts, and so on. Compared with the model group, the destructions were slighter, proliferations of collagen fibers were also fewer, fiber cords were more loosened and comparison of collagen area in Masson staining: The collagen area in the CSM group and FLM group were less than the model of serum SOD was increased obviously in the FLM group (P＜0.05). Conclusion The mechanism of Fuzheng-Liqi mixture in anti-fibrosis effects may be correlated with its anti-lipid peroxidation. Key words: Hepatic fibrosis; Fuzheng-Liqi mixture; Hepatic stellate cell; Lipid peroxidation

Dynamic expression of extracellular signal-regulated kinase in rat liver tissue during hepatic fibrogenesis

To investigate whether extracellular signal-regulated kinase 1 (ERK(1)) is activated and associated with hepatic stellate cell (HSC) proliferation in fibrotic rat liver tissue. Rat hepatic fibrosis was induced by bile duct ligation (BDL). Histopathological changes were evaluated by hematoxylin and eosin staining, and Masson's trichrome method. ERK(1) mRNA in rat liver tissue was determined by reverse transcription-polymerase chain reaction, while the distribution of ERK(1) was assessed by immunohistochemistry. ERK(1) protein was detected by Western blotting analysis. The number of activated HSCs was quantified after alpha smooth muscle actin (alpha-SMA) staining. With the development of hepatic fibrosis, the positive staining cells of alpha-SMA increased obviously, and mainly resided in the portal ducts. Fiber septa and perisinuses were accompanied with proliferating bile ducts. The positive staining areas of the rat livers in model groups 1-4 wk after ligation of common bile duct (12.88% +/- 2.63%, 22.65% +/- 2.16%, 27.45% +/- 1.86%, 35.25% +/- 2.34%, respectively) were significantly larger than those in the control group (5.88% +/- 1.46%, P < 0.01). With the development of hepatic fibrosis, the positive cells of ERK(1) increased a lot, and were mainly distributed in portal ducts, fiber septa around the bile ducts, vascular endothelial cells and perisinusoidal cells. Western blotting analysis displayed that the expression of ERK(1) and ERK(2) protein was up-regulated during the model course, and its level was the highest 4 wk after operation, being 3.9-fold and 7.2-fold higher in fibrotic rat liver than in controls. ERK(1) mRNA was expressed in normal rat livers as well, which was up-regulated two days after BDL and reached the highest 4 wk after BDL. The expression of ERK(1) was positively correlated with alpha-SMA expression (r = 0.958, P < 0.05). The expression of ERK(1) protein and mRNA is greatly increased in fibrotic rat liver tissues, which may play a key role in HSC proliferation and hepatic fibrogenesis.

Relationship between focal adhesion kinase and hepatic stellate cell proliferation during rat hepatic fibrogenesis.

To investigate the dynamic expression of focal adhesion kinase (FAK) protein and FAK mRNA in fibrotic rat liver tissue, and the relationship between FAK and hepatic stellate cell (HSC) proliferation. Rat hepatic fibrosis was induced by bile duct ligation (BDL). Histopathological changes were evaluated by hematoxylin and eosin staining, and by Masson's trichrome method. FAK mRNA in the rat livers was determined by reverse transcription-polymerase chain reaction (RT-PCR), and the distributions of FAK were assessed immunohistochemistrically. The number of activated HSCs was quantified after alpha smooth muscle actin (alpha-SMA) staining. With the development of hepatic fibrosis, the positively stained cells of alpha-SMA increased obviously, which were mainly resided in the portal ducts, fiber septa and perisinuses accompanied with proliferating bile ducts. The positively stained areas of the rat livers in model groups 1 to 4 wk after ligation of common bile duct (12.88+/-2.63%, 22.65+/-2.16%, 27.45+/-1.86%, 35.25+/-2.34%, respectively) were significantly larger than those in the control group (5.88+/-1.46%) (P<0.01). The positive staining for FAK significantly increased, which was mainly situated in portal ducts, fiber septa and around the bile ducts, vascular endothelial cells and perisinusoidal cells. The expression of FAK was positively correlated with alpha-SMA expression (r = 0.963, P<0.05). FAK mRNA expression was obviously up-regulated in the model groups compared to the control group. These data suggest that expressions of FAK protein and mRNA are greatly increased in fibrotic rat livers, which may play an important role in HSC proliferation and hepatic fibrogenesis.