PMID: 

Future Med Chem. 2019 Aug ;11(16):2081-2094. PMID: 31538519

Abstract Title: 

Vanillin protects lipopolysaccharide-induced acute lung injury by inhibiting ERK1/2, p38 and NF-κB pathway.

Abstract: 

Thus far, the anti-inflammatory effect of vanillin in acute lung injury (ALI) has not been studied. This study aimed to investigate the effect of vanillin in lipopolysaccharide (LPS)-induced ALI.Our study detected the anti-inflammatory effects of vanillin by ELISA and western blot, respectively. Pretreatment of mice with vanillin significantly attenuated LPS-stimulated lung histopathological changes, myeloperoxidase activity and expression levels of proinflammatory cytokines by inhibiting the phosphorylation activities of ERK1/2, p38, AKT and NF-κB p65. In addition, vanillin inhibited LPS-induced TNF-α and IL-6 expression in RAW264.7 cells via ERK1/2, p38 and NF-κB signaling.Vanillin can inhibit macrophage activation and lung inflammation, which suggests new insights for clinical treatment of ALI.

read more

PMID: 

J Food Prot. 2019 Mar ;82(3):379-389. PMID: 30785306

Abstract Title: 

Inhibitive Effect of Eugenol and Its Nanoemulsion on Quorum Sensing-Mediated Virulence Factors and Biofilm Formation by Pseudomonas aeruginosa.

Abstract: 

The aim of the present study was to evaluate the quorum sensing (QS) inhibition potential of eugenol and eugenol nanoemulsion against QS-dependent virulence factor production and gene expression, as well as biofilm formation in Pseudomonas aeruginosa. In the current study, eugenol nanoemulsion at a sub-MIC of 0.2 mg/mL specifically inhibited about 50% of the QS-mediated violacein production in Chromobacterium violaceum, as well as the production of N-(3-oxododecanoyl)-l-homoserine lactone (3-oxo-C-HSL) and C-HSL N-acyl homoserine lactone signal molecules, pyocyanin, and swarming motility in P. aeruginosa. The inhibitive effect of eugenol and its nanoemulsion on the expression of the QS synthase genes was concentration dependent, displaying 65 and 52% expression level for lasI, respectively, and 61 and 45% expression level for rhlI, respectively, at a concentration of 0.2 mg/mL. In addition, the inhibitive effect of eugenol and its nanoemulsion on the expression of the rhlA gene responsible for the production of rhamnolipid was also concentration dependent, displaying 65 and 51% expression level for the rhlA gene, respectively, at a concentration of 0.2 mg/mL. Eugenol and its nanoemulsion also displayed 36 and 63% respective inhibition of biofilm formation by P. aeruginosa at the 0.2 mg/mL concentration. Therefore, the nanoemulsion could be used as a novel QS-based antibacterial and antibiofilm agent for the control of harmful bacteria.

read more

PMID: 

Metab Brain Dis. 2019 Aug 23. Epub 2019 Aug 23. PMID: 31444631

Abstract Title: 

The effects of Cinnamaldehyde on early brain injury and cerebral vasospasm following experimental subarachnoid hemorrhage in rabbits.

Abstract: 

The neuroprotective and vasodilatory effects of cinnamaldehyde have been widely studied and documented. On the basis of these findings, we hypothesized that cinnamaldehyde exhibits therapeutic effects on subarachnoid hemorrhage-induced early brain injury and cerebral vasospasm. Thirty-two adult male New Zealand white rabbits were randomly divided into four groups of eight rabbits: control, subarachnoid hemorrhage, subarachnoid hemorrhage + vehicle, and subarachnoid hemorrhage + cinnamaldehyde. An intraperitoneal dose of 50 mg/kg cinnamaldehyde was administered 5 min following an intracisternal blood injection, followed by three further daily injections at identical doses. The animals were sacrificed 72 h after subarachnoid hemorrhage was induced. The cross-sectional areas and arterial wall thicknesses of the basilar artery were measured and hippocampal degeneration scores were evaluated. Treatment with cinnamaldehyde was effective in providing neuroprotection and attenuating cerebral vasospasm after subarachnoid hemorrhage in rabbits. It effectively increased the cross-sectional areas of the basilar artery and reduced the arterial wall thickness; in addition, hippocampal degeneration scores were lower in the cinnamaldehyde group. The findings of this study showed, for the first time to our knowledge, that cinnamaldehyde exhibits neuroprotective activity against subarachnoid hemorrhage-induced early brain injury and that it can prevent vasospasm. Potential mechanisms underlying the neuroprotection and vasodilation were discussed. Cinnamaldehyde could play a role in subarachnoid hemorrhage treatment.

read more

PMID: 

J Histotechnol. 2019 Aug 28:1-10. Epub 2019 Aug 28. PMID: 31460853

Abstract Title: 

Neuro-amelioration of cinnamaldehyde in aluminum-induced Alzheimer's disease rat model.

Abstract: 

Aluminum (Al) is a neurotoxic substance which has played an important role in the etiology, pathogenesis, and development of amyloid-β (Aβ) plaques. This study was carried out to evaluate the neuroprotective effect of aqueous cinnamon extract against aluminum chloride (AlCl)-induced Alzheimer's disease. Forty adult male albino rats, randomly divided into four equal groups. Control group; ACE200 group administered aqueous cinnamon extract (ACE) orally; AlClgroup received daily intraperitoneal (i.p.) injection of AlClfor 60 days to induce neurotoxicity and AlCl+ ACE200 group received a combination of AlCland ACE in the same dose and route as previous groups. Aluminum administration significantly enhanced the memory impairment and the Aβ formation in the rat model. The cerebellum exhibited a significant reduced number of Purkinje cells, marked decrease in the density of dendritic arborization and prominent perineuronal spaces in the molecular layer. There was loss of dendritic spines, neurofibrillary degeneration, and appearanceof neuritic plaques. Concomitant administration of AlCland ACE displayed an observable protection against these changes with progressive improvement in memory and intellectual performance. In conclusion, ACE may play a protective role against formation of amyloid-β plaques in cerebellum.

read more

PMID: 

Eur J Pharmacol. 2019 Jun 5 ;852:14-24. Epub 2019 Feb 20. PMID: 30796902

Abstract Title: 

Anti-oxidant and anti-inflammatory effects of cinnamaldehyde and eugenol on mononuclear cells of rheumatoid arthritis patients.

Abstract: 

Rheumatoid arthritis (RA) is an autoimmune disorder affecting joints and frequently characterized by initial local and later systemic inflammation. The present study was conducted with the aim to determine the anti-inflammatory and antioxidant effects of cinnamaldehyde and eugenol in the peripheral blood mononuclear cells (PBMC) of RA patients. PBMCs obtained from RA patients were treated with varying concentrations of cinnamaldehyde and eugenol. The levels of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) were monitored in the 24-h culture supernatant of PBMCs. Reactive oxygen species formation, biomolecular oxidation and the activities of antioxidant enzymes were also determined. FTIR analysis was done to determine structural alterations in the PBMCs. Molecular docking was performed to gain an insight into the binding mechanism of eugenol and cinnamaldehyde with pro-inflammatory cytokines. The levels of pro-inflammatory cytokines and markers of oxidative stress were found to be elevated in the PBMC culture of RA patients as compared to the healthy controls.Cinnamaldehyde and eugenol have significantly reduced the levels of cytokines. Reactive oxygen species formation, biomolecular oxidation and antioxidant defense response were also ameliorated by treating PBMCs with both the compounds. FTIR results further confirms cinnamaldehyde and eugenol mediated protection to biomolecules of PBMCs of RA patients. Molecular docking results indicates interaction of cinnamaldehyde and eugenol with key residues of TNF-α and IL-6. Cinnamaldehyde and eugenol were found to exert potent anti-inflammatory and anti-oxidant effects on the PBMC culture of RA patients. So, these compounds may be used as an adjunct in the management of RA.

read more

PMID: 

Phytother Res. 2019 May ;33(5):1562-1569. Epub 2019 Apr 1. PMID: 30932261

Abstract Title: 

Eugenol inhibits non-small cell lung cancer by repressing expression of NF-κB-regulated TRIM59.

Abstract: 

In view of the recognized anti-tumor properties of eugenol against non-small cell lung cancer (NSCLC) in cell culture, here we further set out to investigate the potential therapeutic effect of eugenol in vivo and elucidate the underlying molecular mechanism. The relative expression levels of TRIM59 and p65 in NSCLC were quantified by real-time polymerase chain reaction. Xenograft tumor model was established with TRIM59-deficient H1975 cells, and tumor progression was monitored. Kaplan-Meier's analysis was performed to measure overall survival. Protein levels of TRIM59 and p65 in xenograft tumor were determined by western blot. Direct binding of p65 on the TRIM59 promoter was analyzed by chromatin immunoprecipitation assay, and the regulatory effect was interrogated with luciferase reporter assay. Both TRIM59 and p65 were up-regulated in NSCLC. Eugenol treatment significantly inhibited xenograft tumor progression and prolonged the overall survival of tumor-bearing mice. Mechanistically, eugenol suppressed p65 expression, which subsequently decreased TRIM59 expression. TRIM59 deficiency fully recapitulated the anti-tumoral phenotype elicited by eugenol. Ectopic expression of TRIM59 completely abolished the tumor suppressive effect of eugenol, which underlined the predominant role of TRIM59 in mediating the signaling downstream of eugenol treatment. Eugenol inhibited NSCLC via repression NF-κB-TRIM59 pathway.

read more

PMID: 

Arch Physiol Biochem. 2019 Aug 9:1-9. Epub 2019 Aug 9. PMID: 31397187

Abstract Title: 

and its main ingredient, carvacrol, affect on the renal function, histopathological, biochemical and antioxidant parameters in adriamycin-induced nephrotic rats.

Abstract: 

Oxidative stress has a major role in the nephrosis. In the present study, the effects of hydroalcoholic extract of(ZM) and carvacrol (CAR) were evaluated on the renal damage induced by adriamycin (ADR). The animals accidentally divided into four groups including: Control, ADR, ZM + ADR and CAR + ADR. The renal tissue, urine, and blood samples subjected to biochemical markers and histopathological evaluation. ADR significantly decreased glomerular filtration rate (GFR) while escalated urine protein excretion as well as protein clearance ( 

read more

PMID: 

Avicenna J Phytomed. 2019 Sep-Oct;9(5):465-473. PMID: 31516860

Abstract Title: 

could improve hippocampal tau protein and TNFlevels and cognitive behavior defects in a rat model of Alzheimer's disease.

Abstract: 

Objective: (ZM) is a plant with ethnopharmacological value which was recently tested to reduce symptoms of Alzheimer's disease (AD). The aim of the present study was to determine the effect of ZM essential oil on spatial cognitive and noncognitive behavior, as well as hippocampal tau protein and tumor necrosis factor alpha (TNFα) concentrations in rats with AD.Materials and Methods: Thirty-five adult male Sprague Dawley rats (300±30 g) were randomly divided into 5 groups: control (intact rats); sham (received intracerebroventricular (ICV) microinjection of normal saline); AD control (rats with AD that did not receive any treatment); vehicle control (rats with AD that orally received tween-80, 5% (ZM essential oil vehicle)for 20 days) and experimental (rats with AD that orally received ZM essential oil 100 µl/kg/day for 20 days). AD was induced by bidirectional microinjection of β amyloid 1-42 (10 µg/2µl). Tau protein and TNFα concentrations were measured by ELISA methods. Spatial cognitive and noncognitive behavior were determined by Morris water maze (MWM) test.Results: ZM essential oil significantly improved latency time, time spent in the target quarter and cognitive behavior of rats with AD compared to control and sham groups (p

read more

PMID: 

J Cell Physiol. 2019 May ;234(5):6854-6864. Epub 2018 Nov 1. PMID: 30387132

Abstract Title: 

Laurus nobilis leaf extract controls inflammation by suppressing NLRP3 inflammasome activation.

Abstract: 

Laurus nobilis Linn. (Lauraceae), commonly known as Bay, has been used as a traditional medicine in the Mediterranean and Europe to treat diverse immunological disorders. Although the effects of L. nobilis on immunosuppression have been reported, the detailed underlying mechanism remains unclear. In this study, to elucidate the anti-inflammatory mechanism of L. nobilis, we examined the effect of L. nobilis leaf extract on inflammasome activation in mouse bone marrow-derived macrophages. L. nobilis leaf extract inhibited NOD-like receptor pyrin domain-containing 3 (NLRP3) inflammasome activation, which was associated with caspase-1 activation, interleukin-1β secretion, and apoptosis-associated speck-like protein containing a CARD (ASC) pyroptosome complex formation. We also observed that 1,8-cineole, the major component of L. nobilis extract, consistently suppressed NLRP3 inflammasome activation. Furthermore, L. nobilis leaf extract attenuated the in vivo expression of proinflammatory cytokines in an acute lung injury mouse model. Our results provide the first evidence that L. nobilis leaf extract modulates inflammatory signaling by suppressing inflammasome activation.

read more

PMID: 

Int J Mol Sci. 2019 Jul 17 ;20(14). Epub 2019 Jul 17. PMID: 31319552

Abstract Title: 

Suppression of-Induced Skin Inflammation byExtract and Its Major Constituent Eucalyptol.

Abstract: 

Acne is an inflammatory skin disorder in puberty with symptoms including papules, folliculitis, and nodules.() is the main anaerobic bacteria that cause acne. It is known to proliferate within sebum-blocked skin hair follicles.activates monocytic cell immune responses to induce the expression of proinflammatory cytokines. Although the anti-inflammatory function of the() extract (LNE) on several immunological disorders have been reported, the effect of LNE in-mediated skin inflammation has not yet been explored. In the present study, we examined the ability of the LNE to modulate the-induced inflammatory signaling pathway, and evaluated its mechanism. LNE significantly suppressed the expression of-mediated proinflammatory cytokines, such as IL-1β, IL-6, and NLRP3. We also found that LNE inhibited the inflammatory transcription factor NF-κB in response to. In addition, eucalyptol, which is the main constituent of LNE, consistently inhibited-induced inflammatory signaling pathways. Moreover, LNE significantly ameliorated-induced inflammation in a mouse model of acne. We suggest for the first time that LNE hold therapeutic value for the improvement of-induced skin inflammation.

read more