Benzothiadiazole-based non-fullerene acceptors

Phenylpropanoids and their derivatives are plant secondary metabolites widely present in fruits, vegetables, cereal grains, beverages, spices and herbs. They are known to have multifaceted effects which include antimicrobial, antioxidant, anti-inflammatory, antidiabetic, anticancer activities and as well as exhibits renoprotective, neuroprotective, cardioprotective and hepatoprotective effects. Owing to their antioxidant, antimicrobial and photoprotective properties, these compounds have wide application in the food (preservation, packaging films and edible coating), pharmaceutical, cosmetic and other industries such as textile (colorant), biofuel (antioxidant additive) and sensors (sensing biologically relevant molecules). Phenylpropanoids are present in commercially available dietary supplements and skin care products. In this review, we have presented the current knowledge on the biosynthesis, occurrence, biological activities of phenylpropanoids and their derivatives, along with the mechanism of action and their potential applications in various industries.

Phenylpropanoids and its derivatives: biological activities and its role in food, pharmaceutical and cosmetic industries.

Methyl ferulic acid attenuates liver fibrosis and hepatic stellate cell activation through the TGF-β1/Smad and NOX4/ROS pathways.

Flexible organic solar cells: Materials, large-area fabrication techniques and potential applications

Liver fibrosis is an abnormal wound repair response caused by a variety of chronic liver injuries, which is characterized by over-deposition of diffuse extracellular matrix (ECM) and anomalous hyperplasia of connective tissue, and it may further develop into liver cirrhosis, liver failure or liver cancer. To date, chronic liver diseases accompanied with liver fibrosis have caused significant morbidity and mortality in the world with increasing tendency. Although early liver fibrosis has been reported to be reversible, the detailed mechanism of reversing liver fibrosis is still unclear and there is lack of an effective treatment for liver fibrosis. Thus, it is still a top priority for the research and development of anti-fibrosis drugs. In recent years, many strategies have emerged as crucial means to inhibit the occurrence and development of liver fibrosis including anti-inflammation and liver protection, inhibition of hepatic stellate cells (HSCs) activation and proliferation, reduction of ECM overproduction and acceleration of ECM degradation. Moreover, gene therapy has been proved to be a promising anti-fibrosis method. Here, we provide an overview of the relevant targets and drugs under development. We aim to classify and summarize their potential roles in treatment of liver fibrosis, and discuss the challenges and development of anti-fibrosis drugs.

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Liver Fibrosis: Therapeutic Targets and Advances in Drug Therapy.

Hepatoprotective effects of Methyl ferulic acid on alcohol-induced liver oxidative injury in mice by inhibiting the NOX4/ROS-MAPK pathway.

The aim of the present study was to assess the molecular mechanism of ethanol‑induced oxidative stress‑mediated apoptosis in L‑02 liver cells in order to elucidate novel pathways associated with alcoholic liver disease. L‑02 cells were treated with 400 mM ethanol with or without inhibitors. The cell viability was measured by an MTT assay. Cell apoptosis was assessed by flow cytometry and a single‑stranded DNA (ssDNA) assay. Intracellular reactive oxygen species (ROS) production of L‑02 cells was determined using the 2',7'‑dichlorofluorescein‑diacetate dye. The protein expression of c‑Jun N‑terminal kinase (JNK), phosphorylated (p)‑JNK, P38, p‑P38, NADPH oxidase (NOX)1, NOX4, p22phox, B‑cell lymphoma 2 (Bcl‑2) and Bcl‑2‑associated X protein were measured by western blot analysis. The mRNA expression of NOX1, NOX4 and p22phox was measured by reverse transcription polymerase chain reaction analysis. The results indicated that after treatment with various concentrations of ethanol for the indicated durations, L‑02 cells were displayed a significant decrease in cell viability in a dose‑and time‑dependent manner. Ethanol‑induced apoptosis and cell death of L‑02 cells was accompanied by the generation of ROS, elevated expression of NOX, as well as phosphorylation of JNK and P‑38. In addition, increased expression of Bcl‑2 was induced by 400 mM ethanol. Furthermore, treatment with NOX inhibitor attenuated the ethanol‑induced a decrease in cell viability, and an increase in apoptosis and Bcl‑2 expression. In conclusion, ethanol induced apoptosis in the L‑02 hepatocyte cell line via generation of ROS and elevated expression of NOX4. This indicated that activation of JNK and p38 in the mitogen‑activated protein kinase pathway promotes apoptosis in L‑02 cells.

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Lin Shi

Papers

Methyl ferulic acid attenuates liver fibrosis and hepatic stellate cell activation through the TGF-β1/Smad and NOX4/ROS pathways.

Hepatoprotective effects of Methyl ferulic acid on alcohol-induced liver oxidative injury in mice by inhibiting the NOX4/ROS-MAPK pathway.

NOX4/ROS mediate ethanol‑induced apoptosis via MAPK signal pathway in L‑02 cells.

Methyl ferulic acid ameliorates alcohol-induced hepatic insulin resistance via miR-378b-mediated activation of PI3K-AKT pathway.