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Metabolic-associated steatohepatitis (MASH) and pancreatic inflammation are key complications of obesity-related metabolic syndrome. Elevated IL-6; a proinflammatory cytokine, contributes to liver steatosis and pancreatic β-islet cells dysfunction. This study explores pancreatic tissue-resident (tr)NK cells IL-6 receptor (IL-6R) in pancreatic injury in a murine MASH model. MASH models were established using male mice fed a high-fat diet ( ; 60.3% kcal from fat) for 4 weeks and using immunocompromised NOD-SCID IL2rγnull (NSG) mice fed with HFD for 16 weeks and injected with 10 × 10 pancreatic trNK and treated with IL-6R antagonizing antibody on week 12. Biochemical assays assessed serum ALT, AST, lipids, glucose, and insulin levels. Pancreatic injury was analyzed through mRNA expression of Reg1, Reg3, oxidative stress marker of tissue malondialdehyde (MDA) and β-islet cells' proliferation and apoptosis. Fibrotic markers of α-SMA, Collagen-I, and Fibronectin were assessed via RT-PCR and trNK cell activation (CD107a, NKp46, IFN-γ) were assessed by flow cytometry. mice exhibited increased serum cholesterol, triglycerides, fasting blood glucose, and liver injury enzymes. Markers of pancreatic injury of Reg1/Reg3 and pancreatic MDA with β-islet cells apoptosis were significantly elevated compared to littermates' control. These results were accompanied by a decline in trNK counts and activations (P < 0.05). In an adoptive transfer model, NSG mice fed with HFD and transplanted with trNK cells from donors (expressing high IL-6) exhibited similar pancreatic injury markers, whereas those receiving trNK cells from mice pre-treated with an IL-6R antagonist showed marked reductions in Reg1/Reg3 (∼2-fold), MDA (∼1.77-fold), and β-islet cells apoptosis (∼2.2-fold). Moreover, phenotypic characterization of the NSG mice fed an HFD transplanted with IL-6R antagonizing antibody showed an increase in the NK cell activation marker CD107a (∼2.3-fold) and amelioration in pancreatic fibrotic profile of α-SMA mRNA expressions of 1.6 -fold when compared to its counterparts. Our data highlights the importance of IL-6R modulation on trNK cells in remodeling pancreatic tissue after liver injury, emphasizing the liver-pancreas axis as a therapeutic target to prevent pancreatic damage, β-islet cells dysfunction and fibrosis and reduce the risk of diabetes and metabolic syndrome.

Considerable interest has been aroused for thiosemicarbazones and their transition metal complexes because of their wide variety of biological activity. A 2-acetylbenzothiophene 4-cyclohexyl-3-thiosemicarbazone ligand 1 was successfully synthesized. The ligand formed complexes namely [ZnL 2 ] 2 , [CdL 2 ] 3 , [NiL 2 ] 4 , [PdCl 2 HL] 5 and [CuL 2 H 2 O] 2 6 , where HL is the corresponding ligand. The ligand and its complexes were characterized by elemental analyses, Fourier transform infrared (FTIR) spectra, ultraviolet–visible spectroscopy (UV/VIS), nuclear magnetic resonance ( 1 H & 13 C NMR) spectra, single crystal X-ray diffraction analysis, molar conductivity and magnetic moment measurements. The single crystal X-ray diffraction analysis indicated that in the solid state the free ligand exists in the thione form with C=S bond distance 1.74 Å. The elemental analysis results for the complexes are in good agreement with the values calculated for the predicted molecular formulas. The spectroscopic analysis of the zinc(II) 2 , cadmium(II) 3 and nickel(II) 4 complex of 1 indicated that the ligand coordinated to the metal centers as a bidentate ligand through the thiolate sulfur and the azomethine nitrogen to give a distorted square planar arrangement around nickel(II) center and a distorted tetrahedral arrangement around zinc(II) and cadmium(II) center. The Zn–S bond distance is 2.28 Å; while, the Zn–N bond distance is 2.05 Å. Palladium(II) complex 5 showed preference for the thione form of the thiosemicarbazone ligand and the structure of the complex is close to a distorted square planar. The ligand 1 was coordinated with copper(II) ions in the thiol form. The complex 6 was dimeric and the geometry surrounding the copper centers is close to a distorted octahedral. In vitro antimicrobial tests showed that some of the prepared complexes had strong inhibitory effect. The cytotoxic activity was evaluated against human hepatocellular carcinoma cells and Chang liver cells.

Two coordination polymers were prepared by the reaction of terephthalic acid (H 2 TPA) with zinc(II) and copper(II) metal ions. The structures of the prepared polymers were determined by elemental analysis, infrared spectroscopy (FTIR), powder X-ray diffraction (PXRD), and UV‒visible spectroscopy and thermogravimetric analysis (TGA). The obtained data revealed that the polymers exhibit an infinite 1D chain. The FTIR results indicated that the geometries surrounding the zinc(II) and copper(II) centers were close to tetrahedral, and that terephthalic acid (H 2 TPA) was coordinated to the centers in a dibasic tetradentate manner through deprotonated hydroxyl and carbonyl oxygen atoms from both sides of H 2 TPA, forming five-membered chelate rings. The polymers' thermal degradation behavior was examined. The Coats–Redfern method was used to determine the thermodynamic and kinetic characteristics of the thermal deterioration. Under UV light, the polymers' photocatalytic properties for methyl orange degradation were investigated. Investigations were also conducted on the influence of variables on the rate of methyl orange degradation, including the amount of catalyst and pH of the dye solution. However, the polymers that were produced had exceptional photocatalytic activity. When H 2 O 2 was added, the efficiency of degradation increased. The breakdown of MO after 150 min irradiation is 91.79 and 94.98% for Zn(II) and Cu(II) polymers, respectively.