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This study describes the protective effects of piperazine derived compounds against aspirin induced gastric injuries and evaluated the role of nitric oxide, inflammatory cytokines and serum level of aspartate aminotransaminases (AST), alanine aminotransaminases (ALT), high density lipoprotein (HDL) and malondialdehyde (MDA). The oral administration of the compounds at doses 30 and 60 mg/kg protected the gastric against the nectrotizing effects of aspirin. The level of nitric oxide (NO) was elevated in the group pretreated with the compounds. The results also showed that pre-treatment with piperazine compounds has led to the decrease in the amount of MDA and increased the activity of AST, ALT and HDL. In conclusion, pre-treatment with piperazine derived compounds; (E)-2-(1-(2-(piperazin-1-yl)ethylimino)ethyl)phenol (2HP), (E)-4-(1-(2-(piperazin-1-yl)ethylimino)ethyl) benzene-1,3-diol (DHP) and their zinc complexes has provided a significant protection to the gastric from damaging effects of aspirin.

The current study described the synthesis and the in vivo acute oral toxicity evaluations in Sprague Dawley rats. The compounds were characterized by elemental analyses, LC-MS, FTIR, 1H NMR, 13C NMR and UV-visible spectroscopy. In the acute toxicity study, a single administration of the compounds was performed orally to the rats at the single doses of 2000 mg/kg and they were then monitored for possible side effects, mortality or behavioral changes up to 14 days. The serum level of aspartate (AST), alanine aminotransferases (ALT), alkaline phosphate (ALP), triglyceride, high density lipoprotein (HDL), immunoglobulins (GAM) and the C-reactive proteins did not significantly change. The hematological indices white blood cells (WBC), haematocrit (HCT), red blood cells (RBC), mean corpuscular volume (MCV), mean corpuscular haemoglobin concentration (MCHC), and mean corpuscular hemoglobin (MCH) were within the normal range. The renal function indices examined were also within the reference range. Generally, the compounds exhibited low toxic effects as required for further in vivo therapeutic studies.

The compound dichlorido-copper(II)-4-(2-5-bromobenzylideneamino)ethyl) piperazin-1-ium phenolate (CuLBS) was synthesized, characterized and screened for acute toxicity and protective activity against ethanol-induced gastric mucosal injury in rats. Gross microscopic lesions, biochemical and immunological parameters and histochemcial staining of glycogen storage were taken into consideration. Oral administration of CuLBS (30 and 60 mg/Kg) for two weeks dose-dependently flattened gastric mucosa, significantly increased gastric mucus and total acidity, compared with control group (P < 0.01). Serum levels of liver enzymes aspartate (AST) and alanine transaminases (ALT), pro-inflammatory (IL-6 and TNF-α) and anti-inflammatory (IL-10) cytokines in the rats exposed to ethanol induced ulceration have been altered. Administration of CuLBS showed considerable (P < 0.05) protection against ulceration by modulating the acute alterations of cytokines AST, ALT and stomach glycogen. Interestingly, CuLBS did not interfere with the natural release of nitric oxide. CuLBS alone (60 mg/Kg) did not exhibit any ulcerogenic effect as assessed using Adami’s scoring scale. An acute toxicity study showed that rats treated with CuLBS (1,000 and 2,000 mg/Kg) manifested no abnormal signs. These findings therefore, suggested that the gastroprotective activity of CuLBS might contribute in modulating the inflammatory cytokine-mediated oxidative damage to gastric mucosa.

In the title compound, C6H17N32+·2ClO4−, the piperazine ring adopts a chair conformation with the ethylammonium fragment occupying an equatorial position. In the crystal, the dications and perchlorate anions are linked through N—H...O hydrogen bonding and weak C—H...O hydrogen bonding into a three-dimensional supramolecular network.

In the title compound, [CdCl2(C14H21N3O2)], the Schiff base ligand chelates the CdII ion in an N,N,O-tridentate fashion. Two Cl atoms complete a distorted square-pyramidal coordination environment around the metal atom. In the crystal, adjacent molecules are linked through C—H...π interactions into infinite chains along the a axis. The molecules are further connected into a three-dimensional network via N—H...O, N—H...Cl and C—H...Cl interactions. The ethylene group is disordered over two sets of sites in a 0.520 (10):0.480 (10) ratio.

In the title compound, [CdCl2(C13H19N3O)], the CdII ion is pentacoordinated with the N,N,O-tridentate Schiff base 2-{[2-(piperazin-4-ium-1-yl)ethyl]iminomethyl}phenolate ligand and two Cl atoms in a highly distorted square-pyramidal geometry; the piperazine ring adopts a chair conformation. In the crystal structure, adjacent molecules are linked together via N—H...O and N—H...Cl hydrogen bonds, forming infinite layers parallel to the ab plane. The layers are further connected through C—H...Cl interactions into a three-dimensional network.

In the title compound, C20H24N4, the cyclohexane ring adopts a chair conformation with the two imine groups linked at equatorial positions. The two halves of the molecule are related by a crystallographic twofold rotation axis. The dihedral angle between the pyridine rings is 75.73 (3)°.

In the title compound, [CuCl2(C11H17N3)], the CuII ion is five-coordinated with a distorted square-pyramidal configuration. The three N atoms of the Schiff base ligand and one Cl atom are located in the basal plane, whereas the other Cl atom is apically positioned.