RESUMEN
Cardiovascular diseases (CVD) are the primary cause of death globally. Activation of oxidative stress and inflammatory pathways are contributory to the development of CVD. Pharmacological activities of vanillic acid have been investigated suggesting that they may have therapeutic utility clinically. Given its phenolic nature, the anti-inflammatory and antioxidant properties of vanillic acid have been shown to exert potent inhibitory activity against Adenosine Monophosphate-Activated Protein Kinase (AMPK), Nuclear Factor Kappa B (NF- κB), the Janus kinase (JAK)/signal transducer and activator of transcription (STAT), Nod-like receptor family protein (NLRP), Toll-like receptors (TLRs), Mitogen-Activated Signaling Proteins (MAPK) and Mammalian Target of Rapamycin (mTOR) signaling pathways. Vanillic acid has been shown to block pro-inflammatory cytokines and suppress inflammatory cascades. The inhibitory impact of vanillic acid on reactive oxygen species (ROS) and nitric oxygen synthase (iNOS) expression has also been demonstrated. Vanillic acid reduces oxidative-related markers such as superoxide dismutase (SOD), glutathione (GSH), Heme Oxygenase 1 (HO-1), and glutathione peroxidase (GSH-Px). Here, we review the cardioprotective effects and mechanisms of action of vanillic acid in CVD. Current potential applications of vanillic acid in CVD are discussed concerning preclinical and clinical studies.
Asunto(s)
Enfermedades Cardiovasculares , Ácido Vanílico , Humanos , Ácido Vanílico/farmacología , Ácido Vanílico/uso terapéutico , Enfermedades Cardiovasculares/tratamiento farmacológico , Transducción de Señal , FN-kappa B/metabolismo , Antiinflamatorios/farmacología , Estrés Oxidativo , Factor 2 Relacionado con NF-E2/metabolismoRESUMEN
BACKGROUND/AIMS: The aim of present study is to estimate the effects of Melissa officinalis L. (MO) on visceral hypersensitivity (VH), defecation pattern and biochemical factors in 2 experimental models of irritable bowel syndrome (IBS) and the possible role of nitric oxide. METHODS: Two individual models of IBS were induced in male Wistar-albino rats. In the acetic acid model, the animals were exposed to rectal distension and abdominal withdrawal reflex, and the defecation patterns were determined. In the restraint stress model, the levels of TNF-α, myeloperoxidase, lipid peroxidation, and antioxidant powers were determined in the (removed) colon. Rats had been treated with MO, L-NG-nitroarginine methyl ester (L-NAME), aminoguanidine (AG), MO + AG, or MO + L-NAME in the mentioned experimental models. RESULTS: Hypersensitive response to rectal distension and more stool defecation in control rats have been observed in comparison to shams. MO-300 significantly reduced VH and defecation frequency in comparison to controls. VH and defecation pattern did not show significant change in AG + MO and L-NAME + MO groups compared to controls. Also, significant reduction in TNF-α, myeloperoxidase, thiobarbituric acid reactive substances (TBARS), and an increase in antioxidant power in MO-300 group was recorded compared to controls. AG + MO and L-NAME + MO groups showed a reverse pattern compared to MO-300 group. CONCLUSIONS: MO can ameliorate IBS by modulating VH and defecation patterns. Antioxidant and anti-inflammatory properties along with its effect on the nitrergic pathway seem to play important roles in its pharmacological activity.
RESUMEN
Sulfur mustard (SM) as an alkylating and vesicating agent was used for 100 years as a chemical weapon. SM as bi-functional mustard can attacks and alkylates lots of biomolecules. Different cellular mechanism and molecular pathways are responsible for damages to body tissues. Such as DNA damages, oxidative stress, Apoptosis, and inflammation. Sulfur mustard penetrated body organs and induces long term eye, skin, lung, gastrointestinal, urogenital damages and can cause carcinogenic and mutagenic consequences. Currently there is no definitive treatment protocol for SM exposed patients. The goal of treatment is relieving the symptoms with fast healing rate and retrieval of damaged tissues to normal function and appearance in short period of time. Evaluation of proteomics profile in SM-exposed victims has been performed in animal model and human patients. These studies revealed that different protein were involved in the patients with SM damages to skin and lungs. Apolipoprotein A1, type I cytokeratins K14, K16 and K17, S100 calcium-binding protein A8, α1 haptoglobin isoforms, Amyloid A1, albumin, haptoglobin, and keratin isoforms, immunoglobulin kappa chain are defined expressed proteins in the damaged tissues.