Effect of cholinergic denervation on hepatic fibrosis induced by carbon tetrachloride in rats

Lam, Hung-Bun; Yeh, Ching‐Hua; Cheng, Kai‐Chun; Hsu, Chao‐Tien

doi:10.1016/j.neulet.2008.04.048

Cited by 19 publications

(13 citation statements)

References 37 publications

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“…Ten randomly selected septa at low magnification (1009) were scored as follows: 0 = no positive response; 1 = less than 10% of hepatic cells; 2 = 11-20% of hepatic cells; 3 = 21-30% of hepatic cells; 4 = more than 30% of hepatic cells (Lama et al 2008). …”

Section: Immunohistochemistrymentioning

confidence: 99%

Protective effect of quercetin on liver damage induced by biliary obstruction in rats

Kanter

2010

J Mol Hist

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The aim of this study was to evaluate the possible protective effects of quercetin (QE) against cholestatic oxidative stress and liver damage in the common bile duct ligated rats. A total of 24 male Wistar albino rats were divided into three groups: control, bile duct ligation (BDL) and BDL + received QE; each group contain 8 animals. The rats in QE treated groups were given QE (15 mg/kg) once a day intraperitoneally for 4 weeks starting 3 days prior to BDL operation. The changes demonstrating the bile duct proliferation and fibrosis in expanded portal tracts include the extension of proliferated bile ducts into lobules, mononuclear cells, and neutrophil infiltration into the widened portal areas were observed in BDL group. Treatment of BDL with QE attenuated alterations in liver histology. The alpha smooth muscle actin (α-SMA), transforming growth factor beta (TGF-β1) positive cells and the activity of TUNEL in the BDL were observed to be reduced with the QE treatment. The data indicate that QE attenuates BDL-induced cholestatic liver injury, bile duct proliferation, and fibrosis. The hepatoprotective effect of QE is associated with antioxidative potential.

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Section: Immunohistochemistrymentioning

confidence: 99%

Protective effect of quercetin on liver damage induced by biliary obstruction in rats

Kanter

2010

J Mol Hist

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“…BMP6 is involved in the pathophysiology of chronic heart failure (30). Increasing BMP6 expression, induced by TGF activation, promotes tissue fibrosis and new vascular development, as well as inhibiting cell proliferation (22,31,32). The decreased cell viability and increased apoptosis observed in the present study may in part be due to the activation of the TGF-β-BMP signaling pathway, which may be a target for treating cardiac amyloidosis.…”

Section: Discussionmentioning

confidence: 61%

“…TGF-β can induce endothelial cell inflammation, proliferation and migration, and the immune response, as well as enhancing the synthesis of extracellular matrix proteins (20,21). TGF-β and/or BMP6 can promote hepatocyte apoptosis and fibrosis (22). Activation of the TGF-β-BMP signaling pathway promotes neuronal apoptosis in Alzheimer's disease (AD) (23).…”

Section: Discussionmentioning

confidence: 99%

Analysis of gene expression profiling of amyloidogenic immunoglobulin light‑chains on cultured rat cardiomyocytes

Wang

et al. 2020

Exp Ther Med

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The present study aimed to investigate the toxic effects of different amyloidogenic light-chains (LCs) on cardiomyocytes, and demonstrate the differentially expressed genes (DEGs) and signaling pathways that participate in this process. Cultured cardiomyocytes were treated with recombinant κ LC peptide (AL-09) or with serum from a patient diagnosed with multiple myeloma (λ LC) with cardiac involvement. The 6xHis peptide or serum from healthy patients was used as peptide control or serum control, respectively. Cell viability was determined using CCK-8 assay and apoptosis was analyzed by flow cytometry. The DEGs were detected by RNA sequencing (RNA-Seq), followed by Gene Ontology and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses. Changes in gene expression levels were confirmed by reverse transcription-quantitative PCR. The cell viability in the AL-09 peptide-treated (0.2 mg/ml) and patient serum-treated (1:10 dilution) cardiomyocytes decreased to 42 and-72% of the corresponding control groups. The extent of cell apoptosis increased in AL-09-treated cardiomyocytes compared with the control group. RNA-Seq showed 256 DEGs co-existed in the two paired groups, including 127 upregulated and 88 downregulated genes. The KEGG pathways for upregulated expressed genes included the 'TGF-β signaling pathway', the 'Hedgehog signaling pathway', the 'ErbB signaling pathway' and 'lysine degradation'. The higher mRNA expression of bone morphogenetic protein (Bmp) 4, Bmp6, prostaglandin G/H synthase (Ptgs)1, Ptgs2, epiregulin, Tgfa and procollagen-lysine,2-oxoglutarate 5-dioxygenase 2 were confirmed. The KEGG pathways of downregulated expressed genes included genes involved with the 'p53 signaling pathway' and the 'cell cycle'. The mRNA expression levels of E3 ubiquitin-protein ligase CCNB1IP1 showed significant downregulation in the AL-09 peptide group compared with those in the 6xHis peptide group. In conclusion, cardiomyocytes treated with amyloidogenic λ and κ LCs presented with decreased cell viability compared with controls. Cell apoptosis increased in κ LC-treated cells compared with controls. The gene expression profiles associated with transforming growth factor-β-bone morphogenetic protein, the receptor tyrosine-protein kinase erbB-2 signaling pathways, prostaglandins, collagen production, the p53 signaling pathway and the cell cycle were altered in light-chain-treated cardiomyocytes.

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“…Vagotomy eliminated drug-induced activation of TGF-β in the cerebral spinal fluid 14 . Cholinergic denervation decreased TGF-β1 expression in CCl4-induced liver fibrosis in rats 15 . Also, neuropeptides may alter T-cell responses, switching a Th-1 response to a pro-fibrogenic Th-2 response.…”

mentioning

confidence: 90%

Vagotomy attenuates bleomycin-induced pulmonary fibrosis in mice

Song

Liu

Shaheen

et al. 2015

Sci Rep

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The progression of pulmonary fibrosis (PF) entails a complex network of interactions between multiple classes of molecules and cells, which are closely related to the vagus nerve. Stimulation of the vagus nerve increases fibrogenic cytokines in humans, therefore, activation of the nerve may promote PF. The hypothesis was tested by comparing the extent and severity of fibrosis in lungs with and without vagal innervation in unilaterally vagotomized mice. The results show that in vagotomized lungs, there were less collagen staining, less severe fibrotic foci (subpleural, peri-vascular and peri-bronchiolar lesions) and destruction of alveolar architecture; decreased collagen deposition (denervated vs intact: COL1α1, 19.1 ± 2.2 vs 22.0 ± 2.6 ng/mg protein; COL1α2, 4.5 ± 0.3 vs 5.7 ± 0.5 ng/mg protein; p < 0.01, n = 21) and protein levels of transforming growth factor beta and interleukin 4; and fewer myofibroblast infiltration (denervated vs intact: 1.2 ± 0.2 vs 3.2 ± 0.6 cells/visual field; p < 0.05, n = 6) and M2 macrophages [though the infiltration of macrophages was increased (denervated vs intact: 112 ± 8 vs 76 ± 9 cells/visual field; p < 0.01, n = 6), the percentage of M2 macrophages was decreased (denervated vs intact: 31 ± 4 vs 57 ± 9%; p < 0.05, n = 5)]. It indicated that the vagus nerve may influence PF by enhancing fibrogenic factors and fibrogenic cells.

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Effect of cholinergic denervation on hepatic fibrosis induced by carbon tetrachloride in rats

Cited by 19 publications

References 37 publications

Protective effect of quercetin on liver damage induced by biliary obstruction in rats

Protective effect of quercetin on liver damage induced by biliary obstruction in rats

Analysis of gene expression profiling of amyloidogenic immunoglobulin light‑chains on cultured rat cardiomyocytes

Vagotomy attenuates bleomycin-induced pulmonary fibrosis in mice

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