Chinese medicines as a resource for liver fibrosis treatment

Liver fibrosis is a condition of abnormal proliferation of connective tissue due to various types of chronic liver injury often caused by viral infection and chemicals. Effective therapies against liver fibrosis are still limited. In this review, we focus on research on Chinese medicines against liver fibrosis in three categories, namely pure compounds, composite formulae and combination treatment using single compounds with composite formulae or conventional medicines. Action mechanisms of the anti-fibrosis Chinese medicines, clinical application, herbal adverse events and quality control are also reviewed. Evidence indicates that some Chinese medicines are clinically effective on liver fibrosis. Strict quality control such as research to identify and monitor the manufacturing of Chinese medicines enables reliable pharmacological, clinical and in-depth mechanism studies. Further experiments and clinical trials should be carried out on the platforms that conform to international standards

Effectiveness of Chinese herbal medicine in treating liver fibrosis: a systematic review and meta-analysis of randomized controlled trials

<p>Abstract</p> <p>Background</p> <p>The studies on the effectiveness of Chinese herbal medicines (CHM) in treating liver fibrosis (LF) were not consistent. This study aims to systematically review the effectiveness of CHM on treating LF patients.</p> <p>Methods</p> <p>Databases including MEDLINE, AMED, EMBASE, The Cochrane Central Register of Controlled Trials, China National Knowledge Infrastructure, TCMOnline, Chinese Biomedical Literature Database, and Chinese Medical Current Contents were searched up to March 2011. Randomized controlled trials (RCTs) involving LF patients receiving CHM, Western medicine, combined CHM and Western medicine compared with placebo, Western medicine or no intervention were included. LF markers including serum hyaluronic acid (HA), laminin (LN), procollagen type III (PC-III), type IV collagen (IV-C), matrix metalloproteinase (MMP), and tissue inhibitors of metalloproteinase (TIMP) were measured as primary outcomes. Liver biochemistry, including alanine aminotransferase (ALT) and aspartarte aminotransferase (AST), and improvement of related clinical symptoms were measured as secondary outcomes. Risk of bias of allocation sequence, allocation concealment, blinding, incomplete outcome data, selective outcome reporting, and other biases were assessed.</p> <p>Results</p> <p>Twenty-three RCTs with 2123 participants were analyzed in subgroups of types of comparison and study quality. Fifteen studies were graded as good quality. CHM alone and combined with Western medicine showed significant improvements in HA, LN, PC-III and IV-C compared with Western medicine alone. However, there were no significant differences observed between CHM and placebo treatments.</p> <p>Conclusion</p> <p>The current inconclusive results in determining the effectiveness of CHM treatment on LF, due to the poor methodological quality and high heterogeneity of the studies, suggests that large RCTs using standardized Chinese medicine syndrome diagnosis and CHM formulae with longer follow-up are required for further evaluation.</p

Environmental-Friendly Catalytic Oxidation Processes Based on Hierarchical Titanium Silicate Zeolites at SINOPEC

Since it was claimed by EniChem in 1983 for the first time, titanium silicate‐1 (TS‐1) zeolite presented the most delightful catalytic performance in the area of selective organic oxidation reactions. To enhance the mass diffusion property, hierarchical titanium silicate with hollow cavities within crystal was prepared by using a post‐synthesis treatment in the presence of organic template, and then, it was commercially produced and employed in many industrial catalytic oxidation processes, such as propylene epoxidation, phenol hydroxylation, and cyclohexanone ammoximation. Moreover, we also developed several totally novel oxidation reactions on hollow titanium silicate (HTS) zeolite, i.e., Baeyer‐Villiger oxidation of cyclohexanone and chlorohydrination of allyl chloride with HCl and H2O2. In all cases, HTS shows much better catalytic performance than TS‐1, attributing to the mass diffusion intensification by introducing hollow cavities. On the other hand, enormous works on synthesizing hierarchical TS‐1 zeolites with open intracrystalline mesopores have been done via silanization treatment and recrystallization. Based on them, several bulk molecule oxidation processes with tert‐butyl hydroperoxide, such as epoxidation of fatty acid methyl ester (FAME) and large olefins, have been carried out. As a consequence, hierarchical TS‐1 zeolites supply a platform for developing environmental‐friendly catalytic oxidation processes to remarkably overcome the drawbacks of traditional routes

A snoRNA modulates mRNA 3' end processing and regulates the expression of a subset of mRNAs.

mRNA 3' end processing is an essential step in gene expression. It is well established that canonical eukaryotic pre-mRNA 3' processing is carried out within a macromolecular machinery consisting of dozens of trans-acting proteins. However, it is unknown whether RNAs play any role in this process. Unexpectedly, we found that a subset of small nucleolar RNAs (snoRNAs) are associated with the mammalian mRNA 3' processing complex. These snoRNAs primarily interact with Fip1, a component of cleavage and polyadenylation specificity factor (CPSF). We have functionally characterized one of these snoRNAs and our results demonstrated that the U/A-rich SNORD50A inhibits mRNA 3' processing by blocking the Fip1-poly(A) site (PAS) interaction. Consistently, SNORD50A depletion altered the Fip1-RNA interaction landscape and changed the alternative polyadenylation (APA) profiles and/or transcript levels of a subset of genes. Taken together, our data revealed a novel function for snoRNAs and provided the first evidence that non-coding RNAs may play an important role in regulating mRNA 3' processing

Cholesterol-induced macrophage apoptosis requires ER stress pathways and engagement of the type A scavenger receptor

Macrophage death in advanced atherosclerosis promotes necrosis and plaque destabilization. A likely cause of macrophage death is accumulation of free cholesterol (FC) in the ER, leading to activation of the unfolded protein response (UPR) and C/EBP homologous protein (CHOP)–induced apoptosis. Here we show that p38 MAPK signaling is necessary for CHOP induction and apoptosis. Additionally, two other signaling pathways must cooperate with p38-CHOP to effect apoptosis. One involves the type A scavenger receptor (SRA). As evidence, FC loading by non-SRA mechanisms activates p38 and CHOP, but not apoptosis unless the SRA is engaged. The other pathway involves c-Jun NH2-terminal kinase (JNK)2, which is activated by cholesterol trafficking to the ER, but is independent of CHOP. Thus, FC-induced apoptosis requires cholesterol trafficking to the ER, which triggers p38-CHOP and JNK2, and engagement of the SRA. These findings have important implications for understanding how the UPR, MAPKs, and the SRA might conspire to cause macrophage death, lesional necrosis, and plaque destabilization in advanced atherosclerotic lesions

Hepatoprotective effects of berberine on carbon tetrachloride-induced acute hepatotoxicity in rats

Background: Berberine is an active compound in Coptidis Rhizoma (Huanglian) with multiple pharmacological activities including antimicrobial, antiviral, anti-inflammatory, cholesterol-lowering and anticancer effects. The present study aims to determine the hepatoprotective effects of berberine on serum and tissue superoxide dismutase (SOD) levels, the histology in tetrachloride (CCl 4)-induced liver injury.Methods: Sprague-Dawley rats aged seven weeks were injected intraperitoneally with 50% CCl 4 in olive oil. Berberine was orally administered before or after CCl 4 treatment in various groups. Twenty-four hours after CCl 4 injection, serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities, serum and liver superoxide dismutase (SOD) activities were measured. Histological changes of liver were examined with microscopy.Results: Serum ALT and AST activities significantly decreased in a dose-dependent manner in both pre-treatment and post-treatment groups with berberine. Berberine increased the SOD activity in liver. Histological examination showed lowered liver damage in berberine-treated groups.Conclusion: The present study demonstrates that berberine possesses hepatoprotective effects against CCl 4-induced hepatotoxicity and that the effects are both preventive and curative. Berberine should have potential for developing a new drug to treat liver toxicity. © 2010 Feng et al; licensee BioMed Central Ltd.published_or_final_versio

An analytical approach to evaluate point cloud registration error utilizing targets

Point cloud registration is essential for processing terrestrial laser scanning (TLS) point cloud datasets. The registration precision directly influences and determines the practical usefulness of TLS surveys. However, in terms of target based registration, analytical point cloud registration error models employed by scanner manufactures are only suitable to evaluate target registration error, rather than point cloud registration error. This paper proposes an new analytical approach called the registration error (RE) model to directly evaluate point cloud registration error. We verify the proposed model by comparing RE and root mean square error (RMSE) for all points in three point clouds that are approximately equivalent