Combination of L-Arginine and L-Norvaline protects against pulmonary fibrosis progression induced by bleomycin in mice.

Pulmonary fibrosis (PF) progression may be involved with arginine (Arg) metabolism and immune balance. The present study aimed to explore the effects of L-Arginine (L-Arg) and L-Norvaline (L-Nor) on bleomycin (BLM)-induced PF in mice, meanwhile, and observe dynamic changes of Arg metabolism, immune balance and crosstalk between them in PF progression. Followed intratracheal instillation of BLM or saline, Kunming mice were treated orally with saline, L-Arg, L-Nor and L-Arg + L-Nor three times a day.

Role of canonical transient receptor potential channel-3 in acetylcholine-induced mouse airway smooth muscle cell proliferation.

Aims: Canonical transient receptor potential channel-3 (TRPC3)-encoded Ca-permeable nonselective cation channel (NSCC) has been proven to be an important native constitutively active channel in airway smooth muscle cell (ASMC), which plays significant roles in physiological and pathological conditions by controlling Ca homeostasis in ASMC. Acetylcholine (ACh) is generally accepted as a contractile parasympathetic neurotransmitter in the airway. Recently studies have revealed the pathological role of ACh in airway remodeling, however, the mechanisms remain unclear.

TRPC3-mediated Ca(2+) entry contributes to mouse airway smooth muscle cell proliferation induced by lipopolysaccharide.

Airway remodeling is a histopathological hallmark of chronic respiratory diseases that includes airway smooth muscle cell (ASMC) proliferation. Canonical transient receptor potential channel-3 (TRPC3)-encoded nonselective cation channels (NSCCs) are important native constitutively active channels that play significant roles in physiological and pathological conditions in ASMCs. Lipopolysaccharides (LPSs), known as lipoglycans and endotoxin, have been proven to be inducers of airway remodeling, though the mechanisms remain unclear.

(Ethyl-enediamine-κ(2)N,N)bis[2-(pyridin-2-yl-κN)-1,3-imidazol-1-ido-κN(1)]cobalt(III) nitrate monohydrate.

In the title compound, [Co(C(8)H(6)N(3))(2)(C(2)H(8)N(2))]NO(3)·H(2)O, the Co(III) ion is coordinated by four N atoms from two 2-(pyridin-2-yl)-1,3-imidazol-1-ide ligands and two N atoms of ethyl-enediamine in a distorted octa-hedral geometry. In the crystal, classical N-H⋯N(O) and O-H⋯N(O) hydrogen bonds connect all the isolated components together to yield a three-dimensional structure.

Tetra-kis(ethyl pyridine-4-carboxyl-ate-κN)bis-(thio-cyanato-κN)cobalt(II).

In the title complex, [Co(NCS)(2)(C(8)H(9)NO(2))(4)], the Co(II) atom is six-coordinated by four N atoms from four ethyl pyridine-4-carboxyl-ate ligands in the equatorial plane and two N atoms of thio-cyanate ligands in the axial positions, showing a slightly distorted octa-hedral geometry. The structure exhibits disorder in one of the ethyl chains, which was refined using a two-site model with 0.70 (6):0.

Tetra-aqua-bis-(2-methyl-1H-benzimidazolium-1,3-diacetato-κO)cobalt(II) tetra-hydrate.

In the title compound, [Co(C(12)H(11)N(2)O(4))(2)(H(2)O)(4)]·4H(2)O, the Co(II) atom lies on an inversion center and is octa-hedrally coordinated by six O atoms from four water mol-ecules and two monodentate zwitterionic 2-methyl-benzimidazolium-1,3-diacetate ligands. An intra-molecular O-H⋯O hydrogen bond occurs. In the crystal, inter-molecular O-H⋯O hydrogen bonds link the mol-ecules into a three-dimensional network.

(4,5-Diaza-fluoren-9-one-κN,N')bis-(1H-imidazole-κN)bis-(thio-cyanato-κN)cobalt(II).

In the title complex, [Co(NCS)(2)(C(3)H(4)N(2))(2)(C(11)H(6)N(2)O)], the Co(II) atom has a distorted octa-hedral coordination with the N atoms of the 4,5-diaza-fluoren-9-one ligand and two N atoms from imidazole ligands in the equatorial positions and the axial sites occupied by two N atoms of the thio-cyanate ligand. Inter-molecular N-H⋯O hydrogen bonding forms a one-dimensional motif parallel to the cell ab diagonal.

Effects of isoliensinine on proliferation of porcine coronary arterial smooth muscle cells induced by phenylephrine.

Aim: To investigate the inhibitory effects and mechanism of action of isoliensinine (IL) on the proliferation of porcine coronary arterial smooth muscle cells (CASMCs) induced by phenylephrine (Phen) and its mechanisms of action.

Methods: MTT assay, immunohistochemical method and Western blotting were adopted.

Results: IL (0.

Inhibitory effects of isoliensinine on bleomycin-induced pulmonary fibrosis in mice.

The effects of isoliensinine (IL), a bisbenzylisoquinoline alkaloid extracted from the Chinese traditional medicine seed embryo of Nelumbo nucifera Gaertn., on bleomycin (BLM)-induced pulmonary fibrosis in mice were investigated. Seventy-two male Kungming mice were divided randomly into eight groups as BLM-IL10, BLM-IL20, BLM-IL40, BLM-Sal, Sal-IL10, Sal-IL20, Sal-IL40 and Sal-Sal groups.