MicroRNA interplay between hepatic stellate cell quiescence and activation.

Recent progress on targeting ferroptosis for cancer therapy.

Abstract Liver fibrosis is a common pathologic stage of the development of liver failure. It has showed that exosomes loaded with therapeutic circRNAs can be manufactured in bulk by exosome secreted cells in vitro, thus enabling personalized treatment. This study aimed to investigate the role of exosome-based delivery of circDIDO1 in liver fibrosis. Levels of genes and proteins were examined by qRT-PCR and Western blot. Cell proliferation, apoptosis, and cell cycle were analyzed by using cell counting kit-8 (CCK-8) assay, EdU assay, and flow cytometry, respectively. The binding between circDIDO1 and miR-141-3p was confirmed by dual-luciferase reporter, RNA pull-down and RIP assays. Exosomes were isolated by ultracentrifugation, and qualified by transmission electron microscopy (TEM), nanoparticle tracking analysis (NTA) and Western blot. CircDIDO1 overexpression or miR-141-3p inhibition suppressed the proliferation, reduced pro-fibrotic markers, and induced apoptosis as well as cell cycle arrest in hepatic stellate cells (HSCs) by blocking PTEN/AKT pathway. Mechanistically, circDIDO1 acted as an endogenous sponge for miR-141-3p, further rescue experiments showed that circDIDO1 suppressed HSC activation by targeting miR-141-3p. Extracellular circDIDO1 could be incorporated into exosomes isolated from mesenchymal stem cells (MSCs), and transmitted to HSCs to restrain HSC activation. Clinically, low levels of serum circDIDO1 in exosome were correlated with liver failure, and serum exosomal circDIDO1 had a well diagnostic value for liver fibrosis in liver failure patients. Transfer of circDIDO1 mediated by MSC-isolated exosomes suppressed HSC activation through the miR-141-3p/PTEN/AKT pathway, gaining a new insight into the prevention of liver fibrosis in liver failure patients.

https://www.tandfonline.com/doi/pdf/10.1080/10717544.2022.2030428?needAccess=true

Mesenchymal stem cell-originated exosomal circDIDO1 suppresses hepatic stellate cell activation by miR-141-3p/PTEN/AKT pathway in human liver fibrosis

MicroRNA-155 and antiviral immune responses.

Liver fibrosis (LF) is a healing response to wounds resulting in liver injury that can cause liver failure or even cancer without functional prevention. Resveratrol (RSV) has been suggested to exert biological effects against various human diseases. MicroRNA‑20a (miRNA/miR‑20a) has been shown to promote disease progression. The present study aimed to assess the mechanisms through which RSV induces autophagy and activates the miR‑20a‑mediated phosphatase and tensin homolog (PTEN)/PI3K/AKT signaling pathway in LF. First, a rat model of carbon tetrachloride (CCL4)‑induced LF and a cell model of platelet‑derived growth factor (PDGF)‑BB‑stimulated HSC‑T6 cells were established for use in subsequent experiments. Subsequently, RSV at a range of concentrations was injected into the model rats with LF. Indicators related to liver injury, oxidative stress and fibrosis were determined in the rats with LF. The RSV‑treated HSC‑T6 cells were subjected to transfection with miR‑20a mimic and PTEN overexpression plasmid to assess the levels of liver injury and LF. A dual‑luciferase reporter gene assay was performed to verify the binding sites between PTEN and miR‑20a. RSV was found to alleviate LF in rats, and autophagy was enhanced in the rats with LF following RSV treatment. Furthermore, the activation of the PTEN/PI3K/AKT axis attenuated LF, which was reversed by transfection with miR‑20a mimic. RSV reversed the inhibitory effects of miR‑20a on PTEN expression, reducing miR‑20a expression and promoting PTEN, PI3K and p‑AKT protein expression, thus attenuating LF. On the whole, the present study demonstrates that RSV induces autophagy and activates the miR‑20a‑mediated PTEN/PI3K/AKT signaling pathway to attenuate LF. These findings may lead to the development of potential therapeutic strategies for LF.

/pdf/resveratrol-contributes-to-the-inhibition-of-liver-fibrosis-4go5tuiasl.pdf

Resveratrol contributes to the inhibition of liver fibrosis by inducing autophagy via the microRNA‑20a‑mediated activation of the PTEN/PI3K/AKT signaling pathway.

The activation of hepatic stellate cells (HSCs) caused by stimulating factors or fibrogenic cytokines is the critical stage of liver fibrosis. Recent studies have demonstrated the influence of microRNAs (miRNAs or miRs) on HSC activation and transformation; however, the function and underlying mechanisms of miRNAs in HSC activation have not yet been completely clarified. In the present study, transforming growth factor β1 (TGF‑β1) was used to treat human HSC lines (HSC‑T6 and LX2 cells) to simulate the activation of HSCs in vivo and whether the expression of miRNAs in HSCs was affected by TGF‑β1 treatment was examined using a miRNA microarray. It was observed that miR‑141 was one of the most upregulated miRNAs during HSC activation. Functional analyses revealed that miR‑141 knockdown suppressed the viability of HSCs and inhibited the expression levels of pro‑fibrotic markers. In addition, phosphatase and tensin homolog (PTEN), a well‑known suppressor of the AKT/mammalian target of rapamycin (mTOR) pathway, was found to be directly targeted by miR‑141 in HSCs. More importantly, the knockdown of PTEN markedly reversed the suppressive effects of miR‑141 inhibition on the viability of and the expression levels of pro‑fibrotic markers during HSC activation. Finally, it was observed that the downregulation of miR‑141 blocked the TGF‑β1‑induced activation of the AKT/mTOR pathway in HSCs. On the whole, the findings of the present study indicate that miR‑141 inhibition suppresses HSC activation via the AKT/mTOR pathway by targeting PTEN, highlighting that miR‑141 may serve as a novel therapeutic target for liver fibrosis.

https://www.spandidos-publications.com/10.3892/ijmm.2020.4578/download

Downregulation of miR‑141 deactivates hepatic stellate cells by targeting the PTEN/AKT/mTOR pathway.

Our study determines the resistance gene profile of a set of Acinetobacter baumannii hospital isolates. A. baumannii is responsible for nosocomial outbreaks and sporadic infections. We extracted and PCR amplified bacterial DNA isolated from patients with ages below 60 years (23.36%) and above 60 years (76.64%). Most of the patients were admitted in the ICU (36.13%) and pneumology departments (28.47%). Of 164 isolated strains, 16 (9.75%) contained OXA-51, 8 (4.88%) contained OXA-58, and 140 (85.37%) contained both OXA-51 and OXA-23. Additionally, 8 (7.41%) strains containing OXA-58 and 100 (92.59%) strains containing both OXA-51 and OXA-23 showed multidrug-resistance. Drug resistance rates of A. baumannii to amikacin, tobramycin-levofloxacin, and cotrimoxazole were above 90%, while drug resistance rates to ampicillin, cefotetan, cefazolin, cefoperazone, and nitrofurantoin were 100%. In conclusion, we found that isolated strains containing OXA-51 and OXA-23 were more likely to be resistant or have decreased sensitivity to carbapenems.

/pdf/analysis-of-drug-resistant-gene-detection-of-blaoxa-like-5fr2zscu3r.pdf

Analysis of drug-resistant gene detection of blaOXA-like genes from Acinetobacter baumannii.

The objective of this study was to evaluate the association between MDR1 gene polymorphisms and hepatocellular carcinoma (HCC) risk. Genomic DNA of 1431 subjects was extracted from peripheral blood and genotyping was performed using the created restriction site-polymerase chain reaction (CRS-PCR). We found that the c.1465C > T single nucleotide polymorphisms (SNP) increased HCC risk in all genetic models (p   T may contribute to the risk of HCC. No significantly increased HCC risk was detected in c.159G > T SNP. Our data indicated that the genetic variants of MDR1 gene may be a valuable molecular marker for HCC.

Association analysis between MDR1 gene polymorphisms and risk of hepatocellular carcinoma in Chinese population.

Discovery and mechanism of action of Novel Baicalein modified derivatives as potent antihepatitis agent.

The invention discloses a traditional Chinese medicine composition for treating chronic virulent hepatitis b and a preparation method thereof, and belongs to the technical field of Chinese patent medicine for treating hepatitis b According to the technical scheme, the traditional Chinese medicine composition is prepared from the following raw materials in parts by weight: 55-72 parts of astragalus membranaceus, 58-75 parts of salvia miltiorrhiza, 40-56 parts of glossy privet fruit, 40-58 parts of Chinese wolfberry, 40-58 parts of rhizoma smilacis glabrae, 30-52 parts of radix bupleuri, 32-48 parts of poria cocos, 30-52 parts of schisandra chinensis, 30-58 parts of codonopsis pilosula, 28-56 parts of pinellia ternate, 28-58 parts of Chinese yam, 30-46 parts of isatis roots, 32-48 parts of bighead atractylodes rhizome, 30-46 parts of curcuma aromatica, 32-46 parts of radix paeoniae alba, 30-49 parts of oldenlandia diffusa, 32-49 parts of angelica sinensis, 35-46 parts of pericarpium citri reticulatae, 35-50 parts of honeysuckle, 30-44 parts of polygonatum sibiricum and 25-35 parts of coke hawthorn The invention further discloses the preparation method for the traditional Chinese medicine composition for treating chronic virulent hepatitis b The traditional Chinese medicine composition is prepared from traditional Chinese medicinal materials, has no toxic or side effect, and is low in cost Animal experiments and clinical application studies find that the traditional Chinese medicine composition has good anti-HBV activity

Traditional Chinese medicine composition for treating chronic virulent hepatitis b and preparation method thereof

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