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Metixene hydrochloride hydrate mitigates kidney tubulointerstitial fibrosis by inhibiting Smad3 phosphorylation

2026-02-05T18:01:28Z

Title: Metixene hydrochloride hydrate mitigates kidney tubulointerstitial fibrosis by inhibiting Smad3 phosphorylation Author(s): Lee, Kyeong-Min; Hwang, Yeo Jin Abstract: Chronic Kidney disease (CKD), in which renal fibrosis is the defining pathological feature, poses significant global health and economic challenges. Despite its high clinical prevalence, effective therapies to prevent or reverse renal fibrosis remain scarce. Metixene hydrochloride hydrate (MHH), an anticholinergic drug once used for Parkinson's disease, has not been evaluated for renal fibrosis. Here, we investigated whether MHH mitigates renal fibrosis in a unilateral ureteral obstruction (UUO) mouse model and evaluated its effects on transforming growth factor-β1 (TGF-β1) signaling in renal cells. MHH did not affect the cell viability of NRK-49F cells at concentrations ranging from 0.5 to 5 μM. In vitro, MHH effectively suppressed TGF-β1-induced PAI-1 expression (both mRNA and protein) and secretion in renal fibroblasts, as well as PAI-1 secretion and protein expression in renal glomerular endothelial cells. Furthermore, TGF-β1 stimulated the mRNA and protein expressions of key renal fibrotic factors, including collagen type I, fibronectin, and alpha-smooth muscle actin, in NRK-49F cells. MMH significantly inhibited the expression of these renal fibrotic factors in these cells. UUO kidneys exhibited markedly increased tubular atrophy and interstitial fibrosis, as well as increased expression of renal fibrotic markers. MHH treatment significantly mitigated these pathological parameters and expression of renal fibrotic markers. Mechanistically, MHH suppressed TGF-β1-induced Smad3 phosphorylation both in vitro and in vivo. Our findings indicate that MHH exerts potent antifibrotic effects by downregulating the TGF-β1/Smad3 signaling pathway and suppressing the expression of fibrotic factors in renal cells and obstructed kidneys. Therefore, MHH could be repositioned as a therapeutic agent for renal fibrosis in various kidney diseases.

Synthesis of Block Copolymers Through Melt Polymerization for Compatibilizing PLA/PBAT Blends

2026-01-21T18:01:23Z

Title: Synthesis of Block Copolymers Through Melt Polymerization for Compatibilizing PLA/PBAT Blends Author(s): Kwon, Mi Kyung; Lee, Young Jae; Lee, Se Geun; Kim, Sang Gu; Lee, Sung Jun Abstract: Block copolymers, unlike reactive compatibilizers, can stably localize at the interface without reducing biodegradation rate, making them attractive compatibilizers for PLA/PBAT blends. For industrial use, they should be synthesized from commercial PBAT by melt polymerization to lower costs. However, melt polymerization is exposed to ambient moisture, leading to concurrent formation of PLA homopolymer. In this study, PLA-PBAT block copolymers were synthesized by both solution and melt polymerization with different lactide feed ratios. Melt polymerization was performed in an internal mixer as a precursor to reactive extrusion. Products were characterized by NMR, FT-IR, GPC, DSC, and TGA, and performance in blends was evaluated using DSC, SEM, and UTM. Melt samples displayed two cold crystallization peaks. The high-temperature peak corresponded to PLA homopolymer and became more pronounced with increasing lactide feed ratio. This suggests that excess lactide was consumed in homopolymerization. The presence of PLA homopolymer was more clearly observed in DTA than in GPC. In blends, melt samples improved tensile strength gradually with increasing lactide ratio, whereas solution samples showed the highest strength at a 1:1 PBAT-to-lactide ratio. At the ratio, the blend with solution samples exhibited higher tensile strength than that with melt samples. However, this difference was mitigated when melt samples with higher lactide ratios were incorporated at contents of 5 phr or less. The pristine blend formed metastable alpha ' crystals, while melt-sample-containing blends exhibited both alpha and alpha ' structures, with the alpha form becoming more dominant at higher lactide ratios.

Korean red ginseng extract inhibits microplastic translocation via the gut−liver axis by ameliorating alcohol-induced intestinal disruption

2026-02-19T13:10:10Z

Title: Korean red ginseng extract inhibits microplastic translocation via the gut−liver axis by ameliorating alcohol-induced intestinal disruption Author(s): Baek, Su-Min; Lee, Young-Jin; Yim, Jae-Hyuk; Kim, Tae-Un; Kim, Woo Jun; Lee, Seoung-Woo; Kim, Hee-Yeon; Kang, Kyung-Ku; Lee, Kyeong-Min; Choi, Seong-Kyoon; Kim, Sung Dae; Rhee, Man-Hee; Park, Jin-Kyu Abstract: Background Impaired intestinal mucosal barrier in alcoholic liver disease leads to the entry of toxic substances into the liver parenchyma. Ingestion of microplastics (MPs; plastic particles sized <5 mm) can induce inflammation, metabolic disorders, oxidative stress, and cancer. Red ginseng extract (RGE) is a widely used herbal medicine globally. The effects of RGE on the accumulation of MPs and the underlying mechanisms remain unclear. Methods Nine-week-old male wild-type C57BL/6 mice were fed a control liquid diet or ethanol diet with or without MP and RGE. MPs (fluorescent-tagged 2.16-μm polystyrene MP; dose: 0.1 mg/kg body weight) and RGE (dose: 250 or 500 mg/kg body weight) were orally administered five times a week. Results RGE treatment markedly reduced MP accumulation in the liver and intestines. In the intestines, RGE protected tight junctions, as shown by ZO-1 and F-actin expression, and prevented MP translocation into the lamina propria. It also inhibited ethanol- and MP-induced villi fusion, epithelial detachment, and vacuolization. In the liver, RGE attenuated ethanol-mediated steatosis, lobular inflammation, and ballooning degeneration. In vitro , RGE restored tight junction integrity in Caco-2 cells by upregulating ZO-1 while reducing MP accumulation. However, its effect on goblet cell differentiation (MUC-2) in HT-29 cells was minimal, suggesting that in vivo goblet cell regeneration occurred secondarily to tight junction protection. Conclusion Disruption of the gut–liver axis leads to increased translocation of MPs into the lamina propria and their secondary accumulation in the intestines and liver. RGE inhibits the accumulation of MPs by protecting the intestinal epithelial mucosal barrier.

Revisiting Our First Nano Letters Publication

2026-01-21T11:40:14Z

Title: Revisiting Our First Nano Letters Publication Author(s): Kim, Hyunmin; Potma, Eric Abstract: [No abstract available]