The asymmetric unit of the title compound, [Cu(NCS)(2)(C(11)H(17)N(3))], consists of two crystallographically independent mol-ecules. In each mol-ecule, the Cu(II) ion is five-coordinated in a distorted square-pyramidal geometry wherein the basal plane is defined by the N,N',N"-tridentate Schiff base and one N-bound thio-cyanate ligand. The second N-donor thio-cyanate group, located at the apical site, completes the coordination environment. In the crystal, inter-molecular C-H⋯S and C-H⋯N hydrogen bonds link adjacent mol-ecules into infinite layers parallel to the ac plane. Intra-molecular C-H⋯N inter-actions are also observed.
The asymmetric unit of the title compound, [Zn(NCS)(2)(C(13)H(19)N(3)O)], contains two crystallographically independent mol-ecules. In each mol-ecule, the Zn(II) ion is five-coordinated by the N,N',N"-tridentate Schiff base and the N atoms of two thio-cyanate ligands in a distorted square-pyramidal geometry. The two mol-ecules differ mainly in the deviations from the ideal geometry, with τ values of 0.14 and 0.33. In the crystal, inter-molecular C-H⋯S hydrogen bonds are observed. An intra-molecular C-H⋯N hydrogen bond occurs in one of the independent mol-ecules.
In the title compound, [Cu(NCS)(2)(C(13)H(19)N(3)O)], the Cu(II) ion is five-coordinated by the N,N',N''-tridentate Schiff base and the N atoms of two isothio-cyanate ligands in a square-pyramidal geometry. In the crystal, C-H⋯N, C-H⋯O and C-H⋯S inter-actions link adjacent mol-ecules into layers parallel to the ac plane. A weak inter-molecular π-π inter-action occurs between the aromatic rings with a centroid-centroid distance of 3.9412 (9) Å.
In the title compound, [Zn(C(6)H(14)N(2))(2)(H(2)O)(2)]Cl(2), the Zn(II) atom resides on a special position with site symmetry 2/m and is octa-hedrally coordinated by four N atoms from two trans 1,2-diamino-cyclo-hexane ligands and two water O atoms. In the crystal, N-H⋯Cl and O-H⋯Cl hydrogen bonds link the mol-ecules into a two-dimensional network parallel to the bc plane.
In the title compound, [Cd(NCS)(2)(C(11)H(17)N(3))](n), the Cd(II) atom is octa-hedrally coordinated by the N,N',N''-tridentate Schiff base ligand and one terminal thio-cyanate N atom. Two trans-N:S-bridging thio-cyanates complete the N(5)S donor set around the Cd atom. In the crystal, adjacent Cd(II) ions are linked by the thio-cyanate N:S-bridges into polymeric chains along the c axis.
The title compound, [Sn(C(6)H(5))(3)(C(17)H(25)O(3)S)](n), comprises two symmetry-independent five-coordinated triphenyl-tin mol-ecules which are linked by carboxyl-ate bridges into a polymeric chain. The Sn(IV) atom is in a distorted trans-C(3)SnO(2) trigonal-bipyramidal geometry. The presence of two bulky tert-butyl groups on the benzene ring prevents any hydrogen-bonding inter-actions involving the hydroxyl substituents.
The Sn(IV) atom in the title compound, [Sn(CH(3))(2)(C(18)H(11)ClN(2)O(3))], shows a trans-C(2)NO(2)Sn trigonal-bipyramidal coordin-ation; the axial O-Sn-O angle is 155.22 (5)°. The tridentate N'-(5-chloro-2-oxidobenzyl-idene)-3-hydr-oxy-2-naphthohydrazidate dianion is stabilized by an intra-molecular O-H⋯N hydrogen bond.
The Sn(IV) atom in the title compound, [Sn(CH(3))(2)(C(18)H(11)BrN(2)O(3))], shows a distorted cis-C(2)NO(2)Sn trigonal-bipyramidal coordination geometry, with an axial O-Sn-O angle of 155.27 (9)°. The presence of an intra-molecular O-H⋯N hydrogen bond between the amido N atom and hydr-oxy H atom in the Schiff base ligand helps to stabilize the overall mol-ecular structure.
The environment at the Sn(IV) atom in the title compound, [Sn(C(6)H(11))(2)(C(18)H(11)BrN(2)O(3))], is distorted trigonal-bipyramidal, with the two cyclo-hexyl groups and the imino N atom forming the equatorial plane. The axial O-Sn-O angle is 155.97 (9)°. The presence of an intra-molecular O-H⋯N hydrogen bond in the Schiff base ligand helps to stabilize the overall structure.
The pyridine-coordinated Cu(II) atom in the title Schiff base complex, [Cu(C(15)H(11)N(3)O(5))(C(5)H(5)N)], is O,N,O'-chelated by the doubly deprotonated Schiff base ligand. The metal centre is in a square-planar coordination geometry.
In the title compound, [Cu(C(21)H(22)N(2)O(2))], the cyclo-hexyl ring adopts a chair conformation with the two imine groups linked at equatorial positions. The Cu(II) ion is coordinated by two N atoms and two O atoms from the bis-Schiff base ligand in a slightly distorted square-planar geometry. The dihedral angle between the two benzene rings is 45.89 (9)°. The crystal structure is devoid of any classical hydrogen bonds. However, inter-molecular C-H⋯O inter-actions are present and stabilize the structure.
Staphylococci are facultative anaerobes, perfectly spherical un-encapsulated cocci, with a diameter not exceeding 1 micrometer in diameter. Staphylococcus aureus are generally harmless and remain confined to the skin unless they burrow deep into the body, causing life-threatening infections in bones, joints, bloodstream, heart valves and lungs. Among the 20 medically important staphylococci species, Staphylococcus aureus is one of the emerging human pathogens. Streptomycin had its highest potency against Staphylococcus infections despite the likelihood of getting a resistant type of staphylococcus strains. Methicillin-resistant S. aureus (MRSA) is the persister type of Staphylococcus aureus and was evolved after decades of antibiotic misuse. Inadequate penetration of the antibiotic is one of the principal factors related to success/failure of the therapy. The active drug needs to reach the bacteria at concentrations necessary to kill or suppress the pathogen's growth. In turn the effectiveness of the treatment relied on the physical properties of Staphylococcus aureus. Thus understanding the cell integrity, shape and roughness is crucial to the overall influence of the therapeutic agent on S. aureus of different origins. Hence our experiments were designed to clarify ultrastructural changes of S. aureus treated with streptomycin (synthetic compound) in comparison to artonin E (natural compound). In addition to the standard in vitro microbial techniques, we used transmission electron microscopy to study the disrupted cell architecture under antibacterial regimen and we correlate this with scanning electron microscopy (SEM) to compare results of both techniques.
The title compound, [Sn(C(6)H(11))(3)(C(17)H(25)O(3)S)], exists as a monomeric mol-ecule with the Sn(IV) atom in a distorted tetra-hedral C(3)O coordination geometry. The presence of two bulky tert-butyl groups on the carboxyl-ate prevents any hydrogen-bonding inter-actions involving the hy-droxy group.
Vitex pubescens is a Malaysian therapeutic plant employed in traditional drug to remedy a variety of disorders. The purpose of this research is to assess the gastroprotective efficiency of V. pubescens leaves against ethanol-induced gastric hemorrhagic laceration in rats. Animals were randomly allocated into seven groups and pre-treated, separately, with 10% Tween 20 (normal and ulcer control groups), 20 mg/kg omeprazole (reference group), and 62.5, 125, 250, and 500 mg/kg of V. pubescens extract (experimental groups). All animals were sacrificed after another hour. Histological evaluation of the ulcer control group revealed significant injury to the gastric mucosa with edema and leucocyte infiltration of the submucosal layer. PAS staining, showed remarkably intense magenta color, remarkable increase of HSP70 and decrease of Bax proteins in rats pre-treated with plant extracts compared to the ulcer control group. Gastric homogenates revealed a remarkable increase in endogenous antioxidant enzyme activities (CAT, SOD, GSH) and a decrease in the lipid peroxidation level (MDA) in animals pre-treated with V. pubescens extract compared with the ulcer control group. The gastroprotective activity of this plant might be related to increased antioxidant enzymes and decrease lipid peroxidation upsurge of HSP70 and reduced expression of Bax proteins.
The central Cd(II) atom in the trinuclear title compound, [Cd(3)(C(14)H(19)N(2)O(3))(2)(CH(3)COO)(4)], lies on a center of inversion and is bonded to the O atoms of four acetate groups as well as to the phenolate O atoms of the mono-deprotonated Schiff base ligands in a distorted all-trans octa-hedral geometry. Two of the acetate groups function in a μ(2)-bridging mode, while the other two each chelate to the terminal Cd(II) atom and simultaneously bind to the central metal atom in a κ(3)-bonding mode. The Schiff base anions N,O-chelate to the terminal metal atoms. The morpholine ring assumes a chair conformation.
The current study investigated the cytotoxic effect of 3-(5-chloro-2-hydroxybenzylideneamino)-2-(5-chloro-2-hydroxyphenyl)-2,3-dihydroquinazolin-41(H)-one (A) and 3-(5-nitro-2-hydroxybenzylideneamino)-2-(5-nitro-2-hydroxyphenyl)-2,3-dihydroquinazolin-4(1H)-one (B) on MCF-7, MDA-MB-231, MCF-10A and WRL-68 cells. The mechanism involved in apoptosis was assessed to evaluate the possible pathways induced by compound A and B. MTT assay results using A and B showed significant inhibition of MCF-7 cell viability, with IC50 values of 3. 27 ± 0.171 and 4.36 ± 0.219 μg/mL, respectively, after a 72 hour treatment period. Compound A and B did not demonstrate significant cytotoxic effects towards MDA-MB-231, WRL-68 and MCF-10A cells. Acute toxicity tests also revealed an absence of toxic effects on mice. Fluorescent microscopic studies confirmed distinct morphological changes (membrane blebbing and chromosome condensation) corresponding to typical apoptotic features in treated MCF-7 cells. Using Cellomics High Content Screening (HCS), we found that compound A and B could trigger the release of cytochrome c from mitochondria to the cytosol. The release of cytochrome c activated the expression of caspases-9 and then stimulated downstream executioner caspase-3/7. In addition, caspase-8 showed remarkable activity, followed by inhibition of NF-κB activation in A-and B-treated MCF-7 cells. The results indicated that A and B could induce apoptosis via a mechanism that involves either extrinsic or intrinsic pathways.
Drug resistance presents a challenge in chemotherapy and has attracted research interest worldwide and particular attention has been given to natural compounds to overcome this difficulty. Pulchrin A, a new compound isolated from natural products has demonstrated novel potential for development as a drug. The identification of pulchrin A was conducted using several spectroscopic techniques such as nuclear magnetic resonance, liquid chromatography mass spectrometer, infrared and ultraviolet spectrometry. The cytotoxicity effects on CAOV-3 cells indicates that pulchrin A is more active than cisplatin, which has an IC50 of 22.3 μM. Significant changes in cell morphology were present, such as cell membrane blebbing and formation of apoptotic bodies. The involvement of phosphatidylserine (PS) in apoptosis was confirmed by Annexin V-FITC after a 24 h treatment. Apoptosis was activated through the intrinsic pathway by activation of procaspases 3 and 9 as well as cleaved caspases 3 and 9 and ended at the executioner pathway, with the occurrence of DNA laddering. Apoptosis was further confirmed via gene and protein expression levels, in which Bcl-2 protein was down-regulated and Bax protein was up-regulated. Furthermore, the CAOV-3 cell cycle was disrupted at the G0/G1 phase, leading to apoptosis. Molecular modeling of Bcl-2 proteins demonstrated a high- binding affinity, which inhibited the function of Bcl-2 proteins and led to cell death. Results of the current study can shed light on the development of new therapeutic agents, particularly, human ovarian cancer treatments.
Postmenopausal osteoporosis is the commonest cause of osteoporosis. It is associated with increased free radical activity induced by the oestrogen-deficient state. Therefore, supplementation with palm-oil-derived tocotrienols, a potent antioxidant, should be able to prevent this bone loss. Our earlier studies have shown that tocotrienol was able to prevent and even reverse osteoporosis due to various factors, including oestrogen deficiency. In this study we compared the effects of supplementation with palm tocotrienol mixture or calcium on bone biomarkers and bone formation rate in ovariectomised (oestrogen-deficient) female rats. Our results showed that palm tocotrienols significantly increased bone formation in oestrogen-deficient rats, seen by increased double-labeled surface (dLS/Bs), reduced single-labeled surface (sLS/BS), increased mineralizing surface (MS/BS), increased mineral apposition rate (MAR), and an overall increase in bone formation rate (BFR/BS). These effects were not seen in the group supplemented with calcium. However, no significant changes were seen in the serum levels of the bone biomarkers, osteocalcin, and cross-linked C-telopeptide of type I collagen, CTX. In conclusion, palm tocotrienol is more effective than calcium in preventing oestrogen-deficient bone loss. Further studies are needed to determine the potential of tocotrienol as an antiosteoporotic agent.
The two aromatic parts of the title compound, C(16)H(13)ClN(3)O(4), are connected through a conjugated -CH=N-NH-C(O)- fragment, giving an almost planar mol-ecule (r.m.s. deviation 0.08 Å). In the crystal structure, adjacent mol-ecules are linked by N-H⋯O and O-H⋯O hydrogen bonds into a three-dimensional network.