cinnamaldehyde/atrophy

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Cinnamaldehyde regulates H2 O 2 -induced skeletal muscle atrophy by ameliorating the proteolytic and antioxidant defense systems.

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Skeletal muscle atrophy/wasting is associated with impaired protein metabolism in diverse physiological and pathophysiological conditions. Elevated levels of reactive oxygen species (ROS), disturbed redox status, and weakened antioxidant defense system are the major contributing factors toward

NTP toxicology and carcinogenesis studies of trans-cinnamaldehyde (CAS No. 14371-10-9) in F344/N rats and B6C3F1 mice (feed studies).

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Cinnamaldehyde is used in foods, beverages, medical products, perfumes, cosmetics, soaps, detergents, creams, and lotions. Cinnamaldehyde has been used as a filtering agent and a rubber reinforcing agent and is used as a brightener in electroplating processes, as an animal repellent, as an insect

Cinnamaldehyde Enhanced Functional Recovery after Sciatic Nerve Crush Injury in Rats.

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Peripheral nerve injury is a common clinical issue induced by trauma, tumor, and damage caused by treatment. Such factors create chemical and inflammatory alterations at the injury site, which increase nerve deterioration. Thus, minimizing these modifications can lead to nerve protection after

Effects of Cinnamaldehyde on the Cell Wall of A. fumigatus and Its Application in Treating Mice with Invasive Pulmonary Aspergillosis.

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UNASSIGNED The invasive pulmonary aspergillosis is a kind of high incidence of disease with difficulties in treatment, poor prognosis, and high mortality. UNASSIGNED The study aimed to reveal the effect of cinnamaldehyde on the fungal cell wall and verify its efficacy on invasive pulmonary

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

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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

Toxicology and carcinogenesis studies of microencapsulated trans-cinnamaldehyde in rats and mice.

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trans-Cinnamaldehyde is a widely used natural ingredient that is added to foods and cosmetics as a flavoring and fragrance agent. Male and female F344/N rats and B6C3F(1) mice were exposed to microencapsulated trans-cinnamaldehyde in the feed for three months or two years. All studies included

Trans-cinnamaldehyde improves neuroinflammation-mediated NMDA receptor dysfunction and memory deficits through blocking NF-κB pathway in presenilin1/2 conditional double knockout mice.

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A chronic neuroinflammatory response has been considered as a critical pathogenesis promoting neurodegenerative progression in Alzheimer's disease (AD). During neuroinflammatory process, microglia are excessively activated and simultaneously release numerous pro-inflammatory mediators that cause

Neuroprotective effect of trans-cinnamaldehyde on the 6-hydroxydopamine-induced dopaminergic injury.

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The anti-inflammatory and neuroprotective effects of trans-cinnamaldehyde (TCA) were investigated on the inflammatory cells and the dopaminergic degeneration in mice. TCA inhibited the up-regulation of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) in the lipopolysaccharide

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

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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 (AlCl₃)-induced

Deciphering the origin, evolution and physiological function of the subtelomeric aryl-alcohol dehydrogenase gene family in the yeast Saccharomyces cerevisiae.

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Homology searches indicate that Saccharomyces cerevisiae strain BY4741 contains seven redundant genes that encode putative aryl-alcohol dehydrogenases (AAD). Yeast AAD genes are located in subtelomeric regions of different chromosomes, and their functional role(s) remain enigmatic. Here, we show

In vitro and in vivo antimicrobial efficacy of essential oils and individual compounds against Phytophthora parasitica var. nicotianae.

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OBJECTIVE To evaluate the antimicrobial effects of essential oils (EOs) from cassia, basil, geranium, lemongrass, cumin and thyme, as well as their major components, against Phytophthora parasitica var. nicotianae; to investigate morphological changes in hyphae and sporangia in response to treatment

Preventive effect of cinnamon essential oil on lipid oxidation of vegetable oil.

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BACKGROUND Lipid oxidation is the main deterioration process that occurs in vegetable oils. This process was effectively prevented by natural antioxidants. Cinnamomum zeylanicum (Cinnamon) is rich with antioxidants. The present study was conducted to evaluate the effect of cinnamon on

Fumigation with essential oils improves sensory quality and enhanced antioxidant ability of shiitake mushroom (Lentinus edodes).

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Several naturally occurring essential oils were evaluated for their effectiveness in maintaining sensory quality and increasing antioxidant levels and activities in shiitake (Lentinus edodes) mushrooms. Freshly harvested mushrooms were fumigated with 5 μl l(-)(1) clove, cinnamaldehyde and thyme oils

Encapsulation performance of proteins and traditional materials for spray dried flavors.

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The objective of this study was to evaluate the potential of selected proteins as alternative materials for flavor encapsulation by spray drying. Two traditional materials (gum acacia and modified starch) and three proteins (sodium caseinate, whey and soy protein isolates) were used at different

Pronociceptive response elicited by TRPA1 receptor activation in mice.

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Ankyrin-repeat transient receptor potential 1 (TRPA1) is a member of the transient receptor potential (TRP) channel family and it is found in sensory neurons. In the present study, we found that TRPA1 receptor activation with allyl isothiocyanate or cinnamaldehyde caused dose-dependent spontaneous

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