Trichinellosis is a serious disease with no satisfactory treatment. We aimed to assess the effect of myrrh (Commiphora molmol) and, for the first time, thyme (Thymus vulgaris L.) against enteral and encysted (parenteral) phases of Trichinella spiralis in mice compared with albendazole, and detect their effect on inducible nitric oxide synthase (iNOS) expression. Oral administration of 500 mg/kg of myrrh and thyme led to adult reduction (90.9%, 79.4%), while 1,000 mg/kg led to larvae reduction (79.6%, 71.3%), respectively. Administration of 50 mg/kg of albendazole resulted in adult and larvae reduction (94.2%, 90.9%). Positive immunostaining of inflammatory cells infiltrating intestinal mucosa and submucosa of all treated groups was detected. Myrrh-treated mice showed the highest iNOS expression followed by albendazole, then thyme. On the other hand, both myrrh and thyme-treated groups showed stronger iNOS expression of inflammatory cells infiltrating and surrounding encapsulated T. spiralis larvae than albendazole treated group. In conclusion, myrrh and thyme extracts are highly effective against both phases of T. spiralis and showed strong iNOS expressions, especially myrrh which could be a promising alternative drug. This experiment provides a basis for further exploration of this plant by isolation and retesting the active principles of both extracts against different stages of T. spiralis.

Obesity has emerged as a leading cause of death in the last few decades, mainly due to associated cardiovascular diseases. Obesity, inflammation, and insulin resistance are strongly interlinked. Lisofylline (LSF), an anti-inflammatory agent, demonstrated protection against type 1 diabetes, as well as reduced obesity-induced insulin resistance and adipose tissue inflammation. However, its role in mitigating cardiac inflammation associated with obesity is not well studied. Mice were divided into 4 groups; the first group was fed regular chow diet, the second was fed regular chow diet and treated with LSF, the third was fed high fat diet (HFD), and the fourth was fed HFD and treated with LSF. Cardiac inflammation was interrogated via expression levels of TNF α, interleukins 6 and 10, phosphorylated STAT4 and lipoxygenases 12 and 12/15. Apoptosis and expression of the survival gene, AMPK, were also evaluated. We observed that LSF alleviated obesity-induced cardiac injury indirectly by improving both pancreatic β-cell function and insulin sensitivity, as well as, directly via upregulation of cardiac AMPK expression and downregulation of cardiac inflammation and apoptosis. LSF may represent an effective therapy targeting obesity-induced metabolic and cardiovascular complications.

Moxifloxacin HCl (moxi.HCl) is a fourth generation of fluoro-quinolone which has a broad spectrum and
improved anti-bacterial activity over other similar quinolones. Topical gel formulations of moxi.HCl were prepared
by using gel forming agents like Carbopol 934, methyl cellulose (MC), hydroxylpropylmethylcellulose (HPMC),
sodium carboxymethylcellulose (Na CMC) and sodium alginate. Compatibility studies of the drug with these
polymers were performed using DSC and FT-IR techniques. Physical characterizations of moxi.HCl gels including
drug content, pH measurement and rheological parameter like viscosity were studied. In vitro drug release from the
prepared gel and kinetics of release were evaluated. Microbiological studies of moxi.HCl gels were carried out by
using agar plate method against the tested micro-organisms. Wound healing study was performed on wound of mice
infected with S.aeurus and P.aeurginosa and treated with the prepared gels. Results revealed that all the used
polymers in gel preparations are compatible with moxi.HCl. All the prepared gels followed non-Newtonian
(shearing thinning) pseudo-plastic flow. Higher percent cumulative drug release (87.68±2.32%) was obtained from
formula (F3) containing 0.1%w/w moxi.HCl and using 4% w/v HPMC as a gel base after 8 hrs. While, formula (F5)
containing 0.1 %w/w moxi.HCl and using 6%w/v of sodium alginate as a gel base showed the lowest percent
cumulative drug release (50.26±1.98%) after the same time. A slight decrease in the release rate of moxi.HCl was
observed by increasing the concentration of the drug to 0.5%w/w in the prepared gels. The tested formulae (F1-F5)
showed a higher antibacterial activity against S.aeurus and P. aeurginosa. Formula (F3) showed a higher % of
wound healing reached to 100% reduction in wound area after 6 days of topical treatment to mice with S.aeurus
infected wound. Hence from the overall study, it was concluded that moxi.HCl gel would be promising in the
treatment of wounds.

Glycemic fluctuations may play a critical role in the pathogenesis of diabetic complications, such as cardiovascular disease. We investigated whether the oxycarotenoid astaxanthin can reduce the detrimental effects of fluctuating glucose on vascular endothelial cells. Human umbilical venous endothelial cells were incubated for 3 days in media containing 5.5mM glucose, 22 mM glucose, or 5.5mM glucose alternating with 22 mM glucose in the absence or presence of astaxanthin or N-acetyl-L-cysteine (NAC). Constant high glucose increased reactive oxygen species (ROS) generation, but such an effect was more pronounced in fluctuating glucose. This was associated with up-regulated p22(phox) expression and down-regulated peroxisome proliferator activated receptor-γ coactivator (PGC-1α) expression. Astaxanthin inhibited ROS generation, p22(phox) up-regulation, and PGC-1α down-regulation by the stimuli of glucose fluctuation. Fluctuating glucose, but not constant high glucose, significantly decreased the endothelial nitric oxide synthase (eNOS) phosphorylation level at Ser-1177 without affecting total eNOS expression, which was prevented by astaxanthin as well as by the anti-oxidant NAC. Transferase-mediated dUTP nick end labeling (TUNEL) showed increased cell apoptosis in fluctuating glucose. Glucose fluctuation also resulted in up-regulating gene expression of pro-inflammatory mediators, interleukin-6 and intercellular adhesion molecule-1. These adverse changes were subdued by astaxanthin. The phosphorylation levels of c-Jun N-terminal kinase (JNK) and p38 were significantly increased by glucose fluctuations, and astaxanthin significantly inhibited the increase in JNK and p38 phosphorylation. Taken together, our results suggest that astaxanthin can protect vascular endothelial cells against glucose fluctuation by reducing ROS generation.