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Revista Fitos ◽  
2021 ◽  
Vol 15 (4) ◽  
pp. 444-455
Author(s):  
Carlos Rocha Oliveira ◽  
Leonardo Mendes Bella ◽  
Marília Cristina Duarte ◽  
Rodolfo de Paula Vieira

The study evaluated the effects of essential oil from Cymbopogon martini (CMEO) on lipopolysaccharide (LPS)-stimulated human fibroblasts. Samples were collected in Monte Verde, Minas Gerais, Brazil and analyzed by gas chromatography with mass spectrometry. The fibroblasts were cultured in a monolayer using Iscove's medium and stimulated by LPS (1 μg/mL) and incubated for 24 h at 37°C. The cytotoxicity was evaluated by MTT assay and collagen concentration by Sirius red. Collagenase activity, hyaluronic acid, and the concentrations of IL-1β; IL-6; MCP-1 (CCL2), and MIP-1-α (CCL3) were evaluated. The effect of CMEO on the expression of mRNA and the secretion of enzymes in fibroblasts were evaluated by RT-qPCR and ELISA, respectively. CMEO was cytotoxic against fibroblasts, in which 10 μg/mL inhibited 50% of cell viability. When treated with CMEO, the fibroblasts produced more collagen and hyaluronic acid than control cells. When stimulated by LPS, fibroblasts exhibited higher production of IL-6, IL-1β, MCP-1, and MIP-1α than control cells. The study demonstrated the effects of CMEO on the modulation of mediators related to inflammation and decreasing the mRNA and secretion levels of metalloproteinases, revealing to be a promising candidate for anti-aging effects and wound healing treatments.


2021 ◽  
Vol 22 (22) ◽  
pp. 12387
Author(s):  
Vasikar Murugapoopathy ◽  
Philippe G. Cammisotto ◽  
Abubakr H. Mossa ◽  
Lysanne Campeau ◽  
Indra R. Gupta

The extracellular matrix of the bladder consists mostly of type I and III collagen, which are required during loading. During bladder injury, there is an accumulation of collagen that impairs bladder function. Little is known about the genes that regulate production of collagens in the bladder. We demonstrate that the transcription factor Odd-skipped related 1 (Osr1) is expressed in the bladder mesenchyme and epithelium at the onset of development. As development proceeds, Osr1 is mainly expressed in mesenchymal progenitors and their derivatives. We hypothesized that Osr1 regulates mesenchymal cell differentiation and production of collagens in the bladder. To test this hypothesis, we examined newborn and adult mice heterozygous for Osr1, Osr1+/−. The bladders of newborn Osr1+/− mice had a decrease in collagen I by western blot analysis and a global decrease in collagens using Sirius red staining. There was also a decrease in the cellularity of the lamina propria, where most collagen is synthesized. This was not due to decreased proliferation or increased apoptosis in this cell population. Surprisingly, the bladders of adult Osr1+/− mice had an increase in collagen that was associated with abnormal bladder function; they also had a decrease in bladder capacity and voided more frequently. The results suggest that Osr1 is important for the differentiation of mesenchymal cells that give rise to collagen-producing cells.


2021 ◽  
pp. 096032712110529
Author(s):  
Lin Xu ◽  
Chenyan Yang ◽  
Jie Ma ◽  
Xinge Zhang ◽  
Qingzhi Wang ◽  
...  

Background: Nicotinamide phosphoribosyltransferase (NAMPT) catalyzes the rate-limiting step in the salvage pathway of mammalian nicotinamide adenine dinucleotide (NAD+) biosynthesis. Through its NAD+-biosynthetic activity, NAMPT is able to regulate the development of hepatic steatosis and inflammation induced by diet or alcohol. However, the roles NAMPT plays in the development of liver fibrosis remain obscure. Purpose: To investigate the roles of NAMPT-mediated NAD+ biosynthesis in hepatic stellate cell (HSC) activation and liver fibrosis. Research Design: Realtime RT-PCR and western blot analyses were performed to analyze the expression of profibrogenic genes. Sirius red staining was conducted to examine the fibrosis in liver. Mouse liver fibrosis was induced by intraperitoneal injection of carbon tetrachloride (CCl4) 2 times a week for 6 weeks. Adenovirus-mediated NAMPT overexpression or nicotinamide mononucleotide (NMN) administration was carried out to study the effects of elevation of NAD+ levels on protecting CCl4-induced liver fibrosis in mice. LX2 cells or primary HSCs were used to study the role of NAMPT overexpression or NMN treatment in reducing profibrogenic gene expression in vitro. ResultsCCl4 administration suppresses NAMPT expression in liver and reduces hepatic NAD+ content. Tgfβ1 treatment decreases intracellular NAD+ levels and NAMPT expression in LX2 cells. Adenovirus-mediated NAMPT overexpression augments liver NAD+ levels, inhibits HSC activation and alleviates CCl4-induced liver fibrosis in mice. Administration of NMN also suppresses HSC activation and protects against CCl4-induced liver fibrosis in mice. Conclusions: NAMPT-mediated NAD+ biosynthesis inhibits HSC activation and protects against CCl4-induced liver fibrosis.


2021 ◽  
Vol 42 (Supplement_1) ◽  
Author(s):  
J Van Wauwe ◽  
S Craps ◽  
A Zwijsen ◽  
M Beerens ◽  
A Luttun

Abstract Introduction PR-domain containing 16 (Prdm16) has an asymmetric expression pattern in the developing cardiovascular system, including ventricular myocardium, endocardium and arterial endothelial and smooth muscle cell (SMC) layers. Heterozygous PRDM16 mutations in humans have been linked with early-onset cardiomyopathy resulting in heart failure. Myocardial PRDM16-deficiency has been suggested as the culprit for this cardiomyopathy, however embryonic Prdm16 deletion in cardiomyocytes or their progenitors in mice only results in symptomatic cardiac defects upon metabolic stress or ageing. This suggests that Prdm16 loss in other cell types has an important co-contribution in the early heart phenotype seen in patients with causal PRDM16 variants. Purpose To investigate the adjuvant role of non-cardiomyocytes to the heart phenotype caused by Prdm16 deficiency, we used a conditional mouse model in which deletion of Prdm16 occurs in all cells expressing an Sm22-driven Cre recombinase which has a combined activity in cardiomyocyte and non-cardiomyocyte lineages in the heart, including SMCs and pericytes. Methods Mice carrying two Prdm16 alleles with a floxed exon 9 (Prdm16fl/fl) were intercrossed with the Sm22-Cre driver line. Offspring of Sm22Cre+; Prdm16fl/fl and Sm22Cre−; Prdm16fl/fl breeding pairs was monitored for Mendelian inheritance and for signs of (progressive) cardiac dysfunction by echocardiography at 5 and 16 weeks of age. Hearts were isolated and analyzed for RNA expression levels of cardiac stress markers Atrial and Brain Natriuretic Peptide (ANP and BNP) via quantitative RT-PCR and histologically for the appearance of fibrosis through Sirius red-staining. Results Genotyping at 5 weeks of age showed a loss of 60.4% of Sm22Cre+; Prdm16fl/fl offspring. Mice surviving at 5 weeks spontaneously developed signs of left ventricular diastolic and systolic dysfunction, the latter shown by a significantly reduced ejection fraction (EF; 37±3% vs. 61±3% in control Sm22Cre−; Prdm16fl/fl littermates). Cardiac expression levels of ANP and BNP were significantly increased (728-fold and 36-fold, respectively) in Sm22Cre+; Prdm16fl/fl mice which also showed perivascular fibrosis compared to control littermates. At 16 weeks of age, this aberrant cardiac phenotype further progressed (EF: 32±3% vs. 57±4%; ANP: 2,541-fold increase; BNP: 129-fold increase) and in addition to perivascular fibrosis, hearts also showed interstitial fibrosis (Sirius red+ area: 17±2% vs. 3.0±0.4% in control littermates). Conclusion Unlike recently reported mice with a Prdm16 deficiency in cardiomyocytes or their (precursor) lineages, mice with a combined loss of Prdm16 in the cardiomyocytes and certain non-cardiomyocyte lineages feature early mortality and (progressive) signs of severe heart failure. Therefore, Prdm16 expressed by non-cardiomyocytes is indispensable for proper cardiac function and its loss in these cell types co-determines the aberrant cardiac phenotype. FUNDunding Acknowledgement Type of funding sources: Public grant(s) – National budget only. Main funding source(s): Fonds voor Wetenschappelijk Onderzoek Strategic Basic Research pre-doctoral fellowship (1S25817N)KU Leuven Research Coordination grant (C14/19/095)


2021 ◽  
Vol 12 ◽  
Author(s):  
Johannes Chang ◽  
Jonathan Meinke ◽  
Moritz Geck ◽  
Marc Hebest ◽  
Nina Böhling ◽  
...  

Background: Liver cirrhosis is a relevant comorbidity with increasing prevalence. Postoperative decompensation and development of complications in patients with cirrhosis remains a frequent clinical problem. Surgery has been discussed as a precipitating event for decompensation and complications of cirrhosis, but the underlying pathomechanisms are still obscure. The aim of this study was to analyze the role of abdominal extrahepatic surgery in cirrhosis on portal pressure and fibrosis in a preclinical model.Methods: Compensated liver cirrhosis was induced using tetrachlormethane (CCL4) inhalation and bile duct ligation (BDL) models in rats, non-cirrhotic portal hypertension by partial portal vein ligation (PPVL). Intestinal manipulation (IM) as a model of extrahepatic abdominal surgery was performed. 2 and 7 days after IM, portal pressure was measured in-vivo. Hydroxyproline measurements, Sirius Red staining and qPCR measurements of the liver were performed for evaluation of fibrosis development and hepatic inflammation. Laboratory parameters of liver function in serum were analyzed.Results: Portal pressure was significantly elevated 2 and 7 days after IM in both models of cirrhosis. In the non-cirrhotic model the trend was the same, while not statistically significant. In both cirrhotic models, IM shows strong effects of decompensation, with significant weight loss, elevation of liver enzymes and hypoalbuminemia. 7 days after IM in the BDL group, Sirius red staining and hydroxyproline levels showed significant progression of fibrosis and significantly elevated mRNA levels of hepatic inflammation compared to the respective control group. A progression of fibrosis was not observed in the CCL4 model.Conclusion: In animal models of cirrhosis with continuous liver injury (BDL), IM increases portal pressure, and development of fibrosis. Perioperative portal pressure and hence inflammation processes may be therapeutic targets to prevent post-operative decompensation in cirrhosis.


2021 ◽  
Vol 12 ◽  
Author(s):  
Hongwei Han ◽  
Guangda Peng ◽  
Maureen Meister ◽  
Hongwei Yao ◽  
Jenny J. Yang ◽  
...  

Although a few studies show that the use of electronic nicotine delivery systems (ENDS) may ameliorate objective and subjective outcomes in COPD smokers who switched to electronic cigarettes, it is unclear whether e-cigarette exposure alters lung pathological features and inflammatory response in COPD. Here, we employed βENaC-overexpressing mice bearing COPD-like pulmonary abnormality, and exposed them to ENDS. We found that ENDS exposure aggravated airspace enlargement and mucus production in βENaC-overexpressing mice, which was associated with increased MMP12 and Muc5ac, respectively. ENDS exposure to mice significantly increased the numbers of macrophages, particularly in M2 macrophages in bronchoalveolar lavage (BAL) fluid, despite ENDS did not induce M2 macrophage polarization in a cultured murine macrophage cell line (RAW264.7). There were no changes in neutrophils in BAL fluid by ENDS exposure. Multiple cytokine productions were increased including M-CSF, IL-1rα, IL-10, and TGF-β1, in BAL fluid from mice when exposed to ENDS. The Sirius Red staining and hydroxyproline assay showed ENDS-exposed mice displayed enhanced fibrotic phenotypes compared to control mice. In conclusion, ENDS exposure enhances airspace enlargement, mucus secretion, and fibrogenesis in COPD mice. This is associated with increased MMP12, inflammatory responses, and M2 macrophage phenotype. This study provides pre-clinical data implicating that electronic cigarette exposure is not safe in COPD patients who want to replace traditional cigarettes with ENDS.


2021 ◽  
Vol 2021 ◽  
pp. 1-25
Author(s):  
Feifei Nong ◽  
Yuqi Liang ◽  
Shangping Xing ◽  
Huixuan Li ◽  
Xizheng Lin ◽  
...  

Colorectal cancer (CRC) is a common malignant tumor around the world. Studying the unique constitution of CRC patients is conducive to the application of personalized medical treatment for CRC. The most common types of constitution in CRC are cold and heat constitution. A previous study has suggested that the malignant progression in cold and heat constitution CRC are different; however, the mechanism remains unclear. The tumor microenvironment (TME) is likely to vary with each individual constitution, which may affect the tumor growth in different constitutions. The extracellular matrix (ECM), the most important component of TME, plays a critical role in disease progression and outcome in patients with CRC. Moreover, collagen, the major component of the ECM, determines the main functional characteristics of ECM and tissue fibrosis caused by collagen deposition, which is one of the signs of CRC malignant progression. This study aimed to explore the mechanisms leading to different colorectal carcinogenesis paradigms between the cold constitution and heat constitution within the context of ECM collagen deposition. We established the CRC rat models and enrolled 30 CRC patients with cold and heat constitution. The collagen-related parameters were detected by using Sirius red staining combined with polarized light microscope, and expressions of collagen (COL I and COL III) and lysyl oxidase (LOX and LOXL2) were determined using immunohistochemistry, while the mRNA levels of COL1A1, COL3A1, LOX, and LOXL2 were measured by qRT-PCR. We found that a higher degree of collagen deposition in the cold-constitution group. The results suggest cold and heat constitution may affect the colorectal carcinogenesis paradigm by influencing the early collagen deposition in colon tissue. The study may provide an effective idea for clinicians to improve the prognosis of CRC patients with different constitutions.


2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Huajun Tang ◽  
Peiyue Zhang ◽  
Lianlin Zeng ◽  
Yu Zhao ◽  
Libo Xie ◽  
...  

Abstract Background Tubulointerstitial fibrosis (TIF) is one of the main pathological features of various progressive renal damages and chronic kidney diseases. Mesenchymal stromal cells (MSCs) have been verified with significant improvement in the therapy of fibrosis diseases, but the mechanism is still unclear. We attempted to explore the new mechanism and therapeutic target of MSCs against renal fibrosis based on renal proteomics. Methods TIF model was induced by adenine gavage. Bone marrow-derived MSCs was injected by tail vein after modeling. Renal function and fibrosis related parameters were assessed by Masson, Sirius red, immunohistochemistry, and western blot. Renal proteomics was analyzed using iTRAQ-based mass spectrometry. Further possible mechanism was explored by transfected galectin-3 gene for knockdown (Gal-3 KD) and overexpression (Gal-3 OE) in HK-2 cells with lentiviral vector. Results MSCs treatment clearly decreased the expression of α-SMA, collagen type I, II, III, TGF-β1, Kim-1, p-Smad2/3, IL-6, IL-1β, and TNFα compared with model rats, while p38 MAPK increased. Proteomics showed that only 40 proteins exhibited significant differences (30 upregulated, 10 downregulated) compared MSCs group with the model group. Galectin-3 was downregulated significantly in renal tissues and TGF-β1-induced rat tubular epithelial cells and interstitial fibroblasts, consistent with the iTRAQ results. Gal-3 KD notably inhibited the expression of p-Akt, p-GSK3β and snail in TGF-β1-induced HK-2 cells fibrosis. On the contrary, Gal-3 OE obviously increased the expression of p-Akt, p-GSK3β and snail. Conclusion The mechanism of MSCs anti-renal fibrosis was probably mediated by galectin-3/Akt/GSK3β/Snail signaling pathway. Galectin-3 may be a valuable target for treating renal fibrosis.


2021 ◽  
Vol 16 (1) ◽  
pp. 62-78
Author(s):  
Nguyễn Minh Thư ◽  
Lê Văn Trình ◽  
Đặng Minh Thành ◽  
Trương Hải Nhung

Mục tiêu: Nghiên cứu này nhằm đánh giá tính an toàn và hiệu quả của tế bào gốc trung mô trên mô hình chuột tổn thương gan do tắc ống dẫn mật. Phương pháp: Chuột Swiss được tiến hành phẫu thuật thắt ống dẫn mật (BDL) để gây bệnh xơ gan. Sau BDL 07 ngày, chuột được tiêm tế bào gốc trung mô từ mô dây rốn (umbilical cord blood-derived - UCB-MSC) với liều 5 x 105tb/con. Hiệu quả điều trị được đánh giá thông qua tỉ lệ sống chết, các chỉ số sinh hóa (AST, ALT, Albumin) và thay đổi cấu trúc mô học (nhuộm H&E), sự tích lũy collagen trong mô gan (nhuộm Sirius red), sự hoạt hóa tế bào hình sao (nhuộm hóa mô miễn dịch với marker α-SMA). Kết quả: Sau 12 ngày điều trị, so với nhóm đối chứng - PBS, chuột tiêm MSC có tỉ lệ sống cao (100%), giảm tổn thương gan (chỉ số sinh hóa men gan Alb, AST và ALT trung bình lần lượt là 2,016 Dg/L, 432.9 UI/L và 417.7 UI/L), giảm diện tích xơ gan thông qua diện tích hoại tử trung bình là 7.529%, sự tích lũy collagen trong gan trung bình là 1.968% và tỷ lệ dương tính của protein α-SMA là 1.42725%. Kết luận: Bước đầu đánh giá được tính an toàn và hiệu quả điều trị chuột tổn thương gan do tắc ống dẫn mật bằng tế bào gốc trung mô (MSC).


Author(s):  
Qiao X ◽  
◽  
Guo J ◽  
Chen J ◽  
Loron MC ◽  
...  

Background: Glomerulosclerosis is characterized by progressive (myo) fibroblast accumulation and collagen deposition involving profibrotic changes of podocytes and endothelial cells. A profibrotic role of MMP-9 in interstitial fibrosis has been reported. Whether MMP-9 plays a role in glomerulosclerosis is not clear yet. Methods: Mouse glomerulosclerosis model [Adriamycin Nephropathy (AN) model] was induced by a single adriamycin injection (10.2mg/kg, with physiological saline for controls) through tail vein in MMP-9-/- and wild-type control mice of BALB/c background. All animals were sacrificed at 4 weeks after injection. Albuminuria (albumin to creatinine ratio) and calculated GFR were measured. Gomori Trichrome (GT) and Sirius Red (SR) staining were used for assessment of glomerular fibrosis. Profibrotic changes of podocytes or glomerular endothelial cells were examined by confocal microscopy using immunofluorescence staining (IF) of desmin or a-SMA with P-cadherin or VEcadherin. Results: Albuminuria was reduced while GFR was increased in MMP-9-/- AN mice compared with those of wild-type mice. Confocal microscopy showed a significant decrease in podocytes double-stained with P-cadherin and desmin, demonstrating that MMP9-/- AN mice were protected from profibrotic changes in podocytes and glomerular endothelial cells. Glomerulosclerosis was significantly reduced in MMP9-/- AN mice compared to that of WT, as demonstrated by GT and SR staining. Conclusions: MMP-9 contributes to glomerulosclerosis at least in part by causing profibrotic changes in podocytes and glomerular endothelial cells.


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