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Two coordination polymers on the basis of distinct nitrogen-donor ligands and biphenyl-2,2′,5,5′-tetracarboxylic acid H4(o,m-bpta), {[Co2(o,m-bpta)(1,3-bimb)2]·DMF·2H2O}n (1) {1,3-bimb = [1,3-pheny...

The solvothermal reaction between H4L, the rigid 2,6-di(2′,5′-dicarboxylphenyl)pyridine ligand, and Co(NO3)2·6H2O in water and DMF results in generation of a three-dimensional (3 D) coordination polymer (CP), [Co4(L)2(H2O)4]n·4DMF·H2O (1, DMF = N,N-dimethylformamide), with Co(II) ions as nodes. The characterization shows that 1 has a 3 D framework structure based on tetranuclear [Co4(μ1-COO)(μ2-COO)6], whose framework could be simplified into a binodal (3,6)-linked three-dimensional network with point symbol (42·6)2(44·62·88·10). The assessment of its application on sepsis mice was implemented and the detailed mechanism was studied. First, the relative expression of NLRP3 and ASC was detected via real time RT-PCR (reverse transcription-polymerase chain reaction) assay after treatment with 1. Subsequently, the enzyme-linked immunosorbent assay was performed and the IL-18 (interleukin-18) and IL-1β (interleukin-1β) contents were detected after treatment with 1. Molecular docking simulation confirmed that the biological activity came from the hydrogen bond that was formed between carboxyl group and the active site.

In the current research, a new Mn(II)-based coordination polymer, {(NH2Me)2[Mn4(Hntb)4(4,4′-bpy)(OH)2] DMF} (1) have been formed by mixing the ligands of H3ntb (4,4′,4′′-nitrilotris-benzoic) and 4,4′-bpy (4,4′-bipyridine). According to the results of UV detection, complex 1 has strong blue luminescence, which means that it can be used as a fluorescent probe for specific detection of Fe3+ ion in water with a Ksv value of 3.2 × 104 M−1. Furthermore, the treatment activity of the compound on sepsis treatment was assessed and the protentional mechanism was revealed. Firstly, the inflammatory cytokines released into the plasma was measured with ELISA detection kit. Then, the survival rate of the infected animals was recorded after compound treatment.

To investigate the changes of NF-kappa B binding activity, the expression of PPARr and their correlation in the liver of rats with fatty liver disease (FLD) induced by different pathogenic factors and to investigate the molecular mechanism of the inflammation in FLD.40 Wistar rats were randomly divided into 4 groups of ten each: normal group, alcohol group, fat-rich diet group, alcohol adding fat-rich diet group. The rats were sacrificed at the end of the 16th week from the starting day of the experiment. Serum and liver specimens were collected. Histological specimens were stained with HE, SudanIV, and Masson and then studied microscopically. The ultrastructural changes were also checked under an electron microscope. NF-kappa B binding activity and the expression of PPARr mRNA were determined by electrophoretic mobility shift assay (EMSA) and RT-PCR respectively. The correlations between NF-kappa B binding activity and the expression of PPARr and the biochemical indexes were analyzed.Steatosis, inflammation, necrosis and fibrosis were present in livers of the rats of all the experimental groups, and were most severe in the alcohol adding fat-rich diet group. NF-kappa B binding activity was markedly increased in the livers of the alcohol group (142+/-16.32) and of the alcohol adding fat-rich diet group (238+/-19.14) in comparison to the livers of the normal (73+/-9.24, F = 6.36, 17.93) and those of the fat-rich diet group (84+/-10.38, F = 5.96, 16.20). Binding activity was higher in the alcohol adding fat-rich diet group than that in the simple alcohol group, but there was no difference between those of the fat-rich diet and normal groups. The level of PPARr mRNA was lower in the livers of the alcohol, fat-rich diet, alcohol adding fat-rich diet groups (0.2530+/-0.069, 0.3647+/-0.082, 0.1226+/-0.054) than that of the controls (0.8097+/-0.094) (F = 15.43, 7.24, 21.45). NF-kappa B binding activity was correlated positively with the level of serum TNF alpha (r = 0.527, 0.639) and the content of MDA in the liver homogenates (r = 0.723, 0.537), but negatively with the expression of PPARr in the livers of the alcohol and the alcohol adding fat-rich diet groups (r = -0.568, -0.891).The enhanced nuclear factors NF-kappa B binding activity and decreased expression of PPARr play a pivotal role in the inflammatory response of FLD induced by alcohol and fat-rich diet. It may provide a new idea for treating FLD effectively.

To study the expression of peroxisome proliferator activated receptor-gamma (PPARgamma) in the liver of rats with fatty liver disease (FLD) and to explore the role of PPARgamma in the pathogenesis of FLD to provide the basis for using PPARgamma ligand to treat patients with FLD.Forty Wistar rats were divided into 4 groups of ten rats each randomly: normal group (group A), alcohol group (group B), fat-rich diet group (group C), alcohol and fat-rich diet group (group D). The rats were sacrificed at the end of the 16th week from the feeding day. Alanine aminotransferase (ALT), tumor necrosis factor-alfa (TNFalpha) in serum and malondialdehyde (MDA) in liver homogenate were determined; livers were collected for observing pathologic changes by HE, Sudan IV, Masson stain under microscope. The morphologic results were analyzed by picture quantitative analysis technique. The changes of ultrastructure were also examined under electron microscope. The expression of PPARgamma in liver was detected by immunohistochemistry and RT-PCR. The correlations between the expression of PPARgamma and biochemical indexes, and liver histology were analyzed.The steatosis, inflammation, necrosis and fibrosis were present in livers of different experimental groups, especially in livers of alcohol and fat-rich diet group. The content of immunodetectable PPARgamma was decreased remarkably in the livers of model rats (group B-D); the level in alcohol and fat-rich diet group (3.43+/-1.48) was significantly lower than that in normal group (18.34+/-3.73), alcohol group (8.82+/-2.52) and fat-rich diet group (11.73+/-2.51) (all P0.01). The level of PPARgamma mRNA was also lower in the livers of model rats (group B-D) than in livers of controls. The expression of PPARgamma in rat liver correlated negatively with the degree of its inflammation, necrosis and fibrosis, as well as the level of serum TNFalpha and the content of MDA in liver homogenates, but not with steatosis or serum ALT.Decreased expression of PPARgamma may play an important role in the development of hepatocellular inflammation, necrosis and fibrosis of rats with FLD. Thus, activating PPARgamma by its ligand can be anticipated to provide a therapy target for FLD.