C 36 H 26 CoN 9 O, monoclinic, P2 1 /n (no. 14), a =13.3290(5) Å, b =12.5385(5) Å, c =18.3604(8) Å, b =103.007(4)°,Source of material 2-(2-pyridyl)benzimidazole (2-pb) was prepared according to [1]. Otherr eagents were purchased commercially and used as received.Amixture of 2-pb (0.020 g, 0.1 mmol), Co(Ac) 2 × 4H 2 O (0.025 g, 0.1mmol) and 8mLdistilled H 2 Owas sealed in a15ml Teflon-lined stainless steel reactor and heated at 150°C for three days.After coolingtoambient temperature, brown crystals of the title compound were collected and washed with distilled water (yield 32 %). Experimental detailsAllHatoms on Catoms were generated at idealized positions and refined as riding with d(C-H) =0 .93 Å, and U iso (H) = 1.2 U eq (C). Thewater Hatoms were located from difference Fourier maps andr efined as riding atomsw ith d(O-H)=0 .861-0.863Åand U iso =1.5 U eq (O). DiscussionCoordination compounds based on benzimidazolic ligands have attractedmuch attention due to their applications as luminescence and biocidal materials [2].Theacetone solvateofthe titlecomplex wasreported in [2]. The asymmetric unit of the title crystal structure contains one Co(III) ion, three deprotonated 2-pb ligands and one lattice water molecule. In the isolated complex, the Co(III) ion is six-coordinated by nitrogen atomsfrom three different deprotonated 2-pb ligands, forming an octahedron. The 2-pb ligands coordinate the Co(III) ion through imidazole and pyridyln itrogen atoms. The Co-N bond lengths vary from 1.906 (2)

Purpose Previous studies showed that doxycycline (Dox), a matrix metalloproteinase inhibitor, can attenuate chronic intermittent hypoxia (CIH)-induced atrial fibrosis in our rats. On this basis, we further investigated the effects of Dox on CIH-induced atrial electrical remodeling in rats. Methods Rats were randomized into 3 groups: Control group, CIH group, and CIH with Dox treatment (CIH-D) group (n = 30). CIH and CIH-D rats were subjected to CIH 8 h/d for 6 weeks. After collecting the basic parameters of the rats, atrial fibrillation (AF) inducibility, conduction inhomogeneity, and epicardial conduction velocity were examined by vitro cardiac electrophysiology experiments. The expression levels of ion channel subunits in atrium were detected by Western blotting. Whole-cell patch clamp experiments were used to recorded action potential (AP), INa, ICa−L, Ito, and the kinetic parameters. Results Compared to the Control rats, CIH rats showed increased AF inducibility, conduction inhomogeneity, and expression levels of p-RyR2, p-CaMKII, Kv11.1, Kir2.3, KCa3.1, while the epicardial conduction velocity, ICa−L, Ito, and expression levels of Cav1.2, Kv1.5, Kv4.3 were decreased. Dox-treatment significantly improved the expression levels of Kv1.5, Kv4.3 and Kir2.3 in CIH-D rats. Conclusion CIH caused atrial electrical remodeling in our rats, which was improved by Dox treatment. These changes indicated the potential effects of Dox in AF.

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