Protective Effect Of Eugenol Research Articles

Anesthetic effects of eugenol on adult ridgetail white prawn (Exopalaemon carinicauda) and its protective effects under simulated transportation

Anesthesia is a common practice used to improve animal welfare and reduce the negative impacts of stress factors in aquaculture settings. However, few studies have been conducted to investigate the application of anesthetics in ridgetail white prawn (Exopalaemon carinicauda). In the present study, the anesthetic efficacy and protective effects of eugenol in adults of this species were evaluated. When the prawns (n = 5) were immersed in different concentrations of eugenol in the range of 0–240 μL/L for 30 min, the results showed that 180 and 240 μL/L could lead to quick sedative and anesthesia effects with 100% mortality after 30 min exposure, while 30 μL/L failed to induce any sedative and anesthesia effects. Further tests showed that adult individuals were quickly anesthetized by eugenol at a concentration of 60–90 μL/L with a 30 min immersion, while half of the prawns were sedated in 30 μL/L eugenol after 4 h exposure, then recovered at 2 h without any mortality. Furthermore, we checked the water quality parameters after the adult prawns were immersed in four eugenol concentrations (0, 10, 20, 30 μL/L) for 8 h of simulated transportation followed by a 96 h recovery, we found that 30 μL/L eugenol treatment could significantly decrease the ammonia nitrogen concentration, and increased the survival rate at 96 h post recovery. The oxidative responses of the prawns during the 8 h transportation at 30 μL/L eugenol followed by 96 h recovery period were analyzed. The results showed that eugenol administration significantly decreased the malonaldehyde (MDA) concentration and the activities of most antioxidant-related enzymes immediately. The present data indicated that eugenol was an efficient anesthetic, which could be used for long-distance transportation of this species. It exhibited excellent protective effects to improve the animal's welfare by improving water quality and alleviating oxidative stress.

Eugenol improves high-fat diet/streptomycin-induced type 2 diabetes mellitus (T2DM) mice muscle dysfunction by alleviating inflammation and increasing muscle glucose uptake.

Eugenol has been used in dietary interventions for metabolic diseases such as diabetes and obesity. However, the protective effect of eugenol on muscle function in diabetes is unclear. In this study, a high-fat diet (HFD) with a streptozocin (STZ) injection induced type II diabetes mellitus in a mouse model. Oral eugenol lowered blood glucose and insulin resistance of HFD/STZ-treated mice. Eugenol reduced HFD/STZ-induced muscle inflammation and prevented muscle weakness and atrophy. Eugenol administration significantly increased GLUT4 translocation and AMPK phosphorylation in skeletal muscle, thereby enhancing glucose uptake. By silencing the transient receptor potential vanilloid channel 1 (TRPV1) gene in C2C12 myotube cells, eugenol was found to increase intracellular Ca2+ levels through TRPV1, which then activated calmodulin-dependent protein kinase-2 (CaMKK2) and affected AMPK protein phosphorylation. In conclusion, eugenol is a potential nutraceutical for preventing high-glucose-induced muscle impairments, which could be explained by its mediating effects on glucose absorption and inflammatory responses in the muscle.

Protective effect of eugenol from Mesua ferrea on the oxidative damages caused by 5-fluorouracil in PBMC cells

5-Fluorouracil (5-FU), a pyrimidine analogue with fluorine at C5 position, is one of the chemotherapy drugs used to treat various cancers. Though 5-FU is a very promising anticancer drug, it can cause side effects such as coronary thrombosis, intestinal mucositis, cognitive impairment, and anaemia through the generation of free radicals, damages the normal cells and also leads to apoptosis. To overcome such toxic effects of 5-FU, in the present work we have explored the cytoprotective potential of eugenol, the antioxidant active compound available in ethanolic extract of an Indian herbal drug Mesua ferrea . Aim of the present study was to evaluate the cytoprotective effect of eugenol against 5-FU toxicity in peripheral blood mononuclear cells (PBMC). Based on MTT assay, it is noticed that eugenol significantly prevents the toxicity of 5-FU (73%) in PBMC cells. Eugenol has lowered the generation of intra-cellular ROS (20035.5 AU) when compared to 5-FU treated cells (58918.5 AU). Eugenol exhibited remarkable inhibition of lipid peroxidation (43%) and cell membrane damage (LDH release: 488.02 IU/L). Thus, eugenol prevents apoptosis-induced cell death when compared with 5-FU in PBMC cells and hence it can be used to overcome the cytotoxicity caused by 5-FU and it warrants further study.

Protective Effect of Eugenol against Acetaminophen-Induced Hepatotoxicity in Human Hepatocellular Carcinoma Cells via Antioxidant, Anti-Inflammatory, and Anti-Necrotic Potency

BACKGROUND: Overdoses acetaminophen (APAP) could cause acute liver failure, even though it used is for analgesics. APAP could cause hepatotoxicity due to multiple mediators of inflammation and oxidative stress. Eugenol has been reported to have anti-inflammatory and antioxidant activity but its hepatoprotective effect has not been widely reported. AIM: The purpose of this research is to know if eugenol could protect HepG2 cells from APAP. METHODS: HepG2 that induced by APAP as hepatotoxicity cells model was treated by using eugenol at 6.25 and 25 μg/mL. The protective effects of eugenol toward hepatotoxicity were evaluated by determine tumor necrosis factor-α (TNF-α) concentration, apoptotic activity, reactive oxygen species (ROS) level, also cytochrome (CYP)2E1 and GPX gene expression. RESULTS: Eugenol at 6.25 and 25 μg/mL concentration can reduce TNF-α concentration, the apoptotic, necrotic, dead cells, and ROS level. Besides it can increase the gene expression (GPX and CYP2E1). The best hepatoprotective effect was found when using the eugenol at 25 μg/mL. CONCLUSION: Therefore, eugenol can be used to protect HepG2 cells against APAP.

Effect of Sodium Fluoride (NaF) Exposure on Heart: Protective Effect of Eugenol with Reference to the Lipid Metabolic Profiles

Flavonoids are phytochemical compounds found in a variety of plants, fruits, vegetables, leaves, and barks, it offers a wide range of health benefits. Quercetin is a polyphenolic flavonoid that is found in onions, apples, berries, broccoli, grapes, nuts, cherries and many other food products. Pharmacologically, quercetin has been examined for various disorders and is reported to possess the ability to prevent as well as treat them. It possesses anti-oxidant, anti-allergic, anti-inflammatory, anti-viral and anti-cancer activity as well. Developing suitable formulation for the delivery of quercetin to specific site leads to better compliance and effective treatment of the disease. This review article highlights the beneficiary activities exhibited by quercetin along with the mechanism behind its activity, followed by reporting the different quercetin formulations developed in last few years.

Protective effect of eugenol on hepatic inflammation and oxidative stress induced by cadmium in male rats

BackgroundCadmium is one of the most toxic heavy metals. The prolonged exposure of it can lead to severe alterations and damage in different tissues including blood, liver, kidney and brain. Eugenol, a phenolic compound, is present in various aromatic plants. It acts as a natural antioxidant and anti-inflammatory agent. The aim of this study was to investigate whether the treatment of eugenol is beneficial against the hepatic oxidative stress and inflammation induced by Cd. MethodsTo study the effect of eugenol in reversal of Cd toxicity, 24 albino rats were equally divided into four different groups: G1 Control (saline), G2 Eugenol (3 mg kg−1), G3 CdCl2 (5 mg kg−1) and G4 CdCl2 + Eugenol (5 mg kg−1 + 3 mg kg−1). All the groups were treated with gavage orally for the period of 21 days. After this treatment period, rats were sacrificed and liver tissues were removed. The hepatic antioxidant status was evaluated by measuring the activities of SOD, Catalase and GST enzymes. The reduced glutathione, lipid peroxidation, protein carbonyl oxidation (PCO) and thiol contents were measured in hepatic tissues. The activities of liver marker enzymes such as ALT, AST, GGT, ALP, TP, albumin, Bilirubin content and LDH were determined to assess the hepatic damage in different groups. Cd induced hepatic inflammation was determined by evaluating the levels of TNF-a, IL-6 and NO. ResultsOral intoxication of Cd for 21 days significantly elevated the level of hepatic markers including activities of LDH, GGT, ALP, ALT, AST and Bilirubin level. The albumin content, reduced GSH level, and activities of antioxidant enzymes were significantly reduced in Cd treated group. The levels of inflammatory markers were significantly elevated in Cd treated group. The eugenol treatment was very effective and it significantly reversed the Cd induced biochemical alterations almost similar to that of control. ConclusionThe results demonstrated that the eugenol possessed very strong anti-oxidative and anti-inflammatory potential. The co-treatment of eugenol with Cd exhibited protective potential of eugenol against Cd induced toxicity. Eugenol was able to improve the cellular redox system in rats treated with Cd.

Histological and Anti-oxidative Effects of Eugenol on Aluminium Chloride-Induced Neurotoxicity in Wistar Rats

Accumulation of aluminium chloride results in damage to different brain regions, and has been used to model damage to the hippocampus which can be associated with various neurodegenerative diseases such as Alzheimer’s and Parkinson’s. The aim of this study was to assess the protective effects of eugenol on aluminium induced neurotoxicity in the hippocampus of adult Wistar rats. 30 adult Wistar rats were procured and divided into six groups with five animals in each group, namely: EGH (300 mg/kg eugenol), EGL (150 mg/kg eugenol), EGH+AL (300 mg/kg eugenol and 100 mg/kg AlCl3), EGL+AL (150 mg/kg eugenol and 100 mg/kg AlCl3), AL (100 mg/kg AlCl3) and CTRL (2 mL/kg distilled water). All Groups were treated orally for 21 days after which they were humanely sacrificed under 0.8 mL/kg ketamine as an anaesthetizing agent. Thereafter, brain tissues were removed and processed for histological demonstration, while the frontal lobe was homogenized and the resultant homogenate obtained was used to assay the levels of superoxide dismutase (SOD) activity. Rat body weights were measured before and after treatment. Aluminium resulted in a significant (p<0.05) reduction in SOD activities. There was alteration in the histology of hippocampal neurons (CA1) and a significant (p<0.01) reduction in body weight of animals. However, the administration of Eugenol was able to restore the activity of SOD. The use of Eugenol offers a promising prospect in the management of neurodegenerative diseases associated with aluminium toxicity.

Protective Effects of Eugenol against Hepatotoxicity Induced by Arsenic Trioxide: An Antileukemic Drug.

Arsenic trioxide (As2O3) has shown effectiveness in the treatment of leukemia, but it is also associated with hepatotoxicity. Given antileukemic drug-induced oxidative stress and toxicity, this study focused on the mitigatory role of eugenol, a monoterpene compound from clove oil, in the hepatic tissue of Wistar rats. Twenty-four male Wistar rats (180-250 g) were randomly divided into 4 groups (6 rats per group): normal control rats, rats treated with As2O2 (4 mg/kg bwt), rats treated with eugenol (5 mg/kg bwt), and rats receiving co-treatment with As2O3 (4 mg/kg bwt) and eugenol (5 mg/kg bwt), all of which orally administered for a period of 30 days. The Tukey test (Origin version 7, Origin Lab Corporation, Northampton, USA) was applied to analyze the one-way analysis of variance (ANOVA) between the different groups. A P value less than 0.05 was considered significant. Oral administration of As2O3 significantly induced hepatic damage, evident from increased levels of aspartate transaminase and alanine transaminase (P=0.01 and P<0.001, respectively). Moreover, a decrease in the activities of enzymatic and nonenzymatic antioxidants altered electrolyte concentration and increased the rate of lipid peroxidation (P=0.04) and the level of nitric oxide (P=0.01). Accumulation studies and histopathological analyses confirmed the biochemical variations. Co-treatment with eugenol (5 mg/kg bwt) exhibited hepatoprotective effects as manifested by the decreased rate of arsenic accumulation, lipid peroxidation, and nitric oxide level along with normalized levels of antioxidants and maintained histology of the liver. Eugenol may be used in combination with arsenic trioxide in chemotherapy to reduce oxidative damage to the hepatic system.

Protective effect of eugenol against restraint stress-induced gastrointestinal dysfunction: Potential use in irritable bowel syndrome

Context: Eugenol, an essential constituent found in plants such as Eugenia caryophyllata Thunb. (Myrtaceae) is reported to possess neuroprotective and anti-stress activities. These activities can potentially be useful in the treatment of stress-induced irritable bowel syndrome (IBS).Objective: The protective effect of eugenol was assessed against restraint stress (RS)-induced IBS-like gastrointestinal dysfunction in rats. Further, its centrally mediated effect was evaluated in this model.Materials and methods: Eugenol (12.5, 25, and 50 mg/kg), ondansetron (4.0 mg/kg, p.o.), and vehicle were administered to rats for 7 consecutive days before exposure to 1 h RS. One control group was not exposed to RS-induction. The effect of eugenol (50 mg/kg) with and without RS exposure was evaluated for mechanism of action and per se effect, respectively. The hypothalamic–pituitary–adrenal cortex (HPA)-axis function was evaluated by estimating the plasma corticosterone level. The levels of brain monoamines, namely serotonin, norepinephrine, dopamine, and their metabolites were estimated in stress-responsive regions such as hippocampus, hypothalamus, pre-frontal cortex (PFC), and amygdala. Oxidative damage and antioxidant defenses were also assessed in brain regions.Results: Eugenol (50 mg/kg) reduced 80% of RS-induced increase in fecal pellets similar to that of ondansetron. Eugenol attenuated 80% of stress-induced increase in plasma corticosterone and modulated the serotonergic system in the PFC and amygdala. Eugenol attenuated stress-induced changes in norepinephrine and potentiated the antioxidant defense system in all brain regions.Conclusion: Eugenol protected against RS-induced development of IBS-like gastrointestinal dysfunction through modulation of HPA-axis and brain monoaminergic pathways apart from its antioxidant effect.

Differential effects of eugenol against hepatic inflammation and overall damage induced by ischemia/re-perfusion injury

Liver injuries, liver tumor resection, and liver transplantation are known to be responsible for ischemia/reperfusion (I/R) injury that, in turn, gives rise to liver damage. This study was undertaken to investigate the possible protective effect of eugenol against the damage induced by I/R in rat livers as well as to explore possible mechanisms of action. Male rats were divided into four groups: sham-operated, I/R only, and two groups that received 10 or 100 mg eugenol/kg/day (Eug10 and Eug100, respectively) for 15 days by gavage and were then subjected to I/R, i.e. an ischemia induced for 45 min followed by re-perfusion for 6 h. The rats were euthanized and liver tissues and blood collected for examination. The results showed that I/R induced massive hepatic structural and functional damage. Eug10-treated rats had improvement in both liver function and structure, and inhibition of I/R-induced increases in serum myeloperoxidase (MPO), tumor necrosis factor (TNF)-α, as well as hepatic nuclear factor-κB (NF−κB) p65 and caspase-3 expression. Eug10 treatment also inhibited the degree of loss in reduced glutathione (GSH) and of rise in malondialdehyde (MDA) levels in liver tissues induced by I/R. In contrast, augmentation of liver damage induced by I/R was noted in Eug100-treated rats, with these hosts displaying significant increases in oxidant, inflammatory, and apoptotic markers relative to levels seen in I/R-only rats. The results of the present study provide the first evidence that a low dose of eugenol may protect the liver against I/R injury in part by decreasing levels of lipid peroxidation, down-regulating inflammatory mediators, and inhibiting apoptosis, and that a larger dose amplifies the liver injury via oxidant and inflammatory effects.

Protective effects of eugenol against oxidized LDL-induced cytotoxicity and adhesion molecule expression in endothelial cells

Eugenol, a natural constituent of a number of aromatic plants and their essential oil fractions, has several biological effects. However, its protective effects against endothelial injury remain unclarified. This study investigates how eugenol affects human umbilical vein endothelial cells (HUVECs) dysfunction mediated by oxidized low density lipoprotein (oxLDL). Our results showed that the suppression of endothelial NO synthase (eNOS) expression, enhancement of adhesion molecules (ICAM, VCAM, and E-selectin) expression, and adherence of monocytic THP1 cells caused by a non-cytotoxic concentration (100 μg/ml) of oxLDL were ameliorated following a eugenol treatment (12.5–100 μM) in HUVECs. Eugneol also inhibited the reactive oxygen species (ROS) generation , intracellular calcium accumulation, and the subsequent mitochondrial membrane potential collapse, cytochrome c release and caspase-3 activation induced by oxLDL. The cytotoxicity and apoptotic features induced by a cytotoxic concentration (200 μg/ml) of oxLDL was also attenuated by eugenol. Our results suggest that eugenol may protect against the oxLDL-induced dysfunction in endothelial cells.

Eugenol: a dual inhibitor of platelet-activating factor and arachidonic acid metabolism

Eugenol is an active principal and responsible for several pharmacological activities of clove oil. We studied the effects of eugenol on human platelet aggregation, arachidonic acid (AA) and platelet-activating factor (PAF) metabolism and in vivo effects on AA and PAF-induced shock in rabbits. Eugenol strongly inhibited PAF-induced platelet aggregation with lesser effect against AA and collegen. The IC(50) values were against AA: 31 ± 0.5; collagen: 64 ± 0.7 and PAF 7 ± 0.2 μM (n=9) respectively. In addition, eugenol stimulated PAF-acetylhydrolase activity suggesting that inhibition of PAF could be due to its inactivation to lyso-PAF. Pretreatment of rabbits with eugenol (50-100 mg/kg) prevented the lethal effects of intravenous PAF (11 μgg/kg) or AA (2 mg/kg) in a dose-dependent fashion. The protective effects of eugenol in the rabbits, however, were more pronounced against PAF-induced mortality (100% protection). In addition, eugenol also inhibited AA metabolism via cyclooxygenase and lipoxygenase pathways in human platelets. Both the production of thromboxane-A(2) and 12-hydroxy-eicosatetraenoic acid was inhibited by eugenol in a concentration-related manner (30-120 μM). In vivo, eugenol (50-100 mg/kg; i.p.) inhibited carrageenan-induced rat paw oedema (P < 0.001). In this test, eugenol was 5 times more potent than aspirin. These results provide evidence that eugenol acts as a dual antagonist of AA and PAF.

The protective effects of eugenol on carbon tetrachloride induced hepatotoxicity in rats.

Our earlier studies in vitro have shown that eugenol inhibits liver microsomal monooxygenase activities and carbon tetrachloride (CCl4)-induced lipid peroxidation (Free Rad. Res. 20, 253-266, 1994). The objective of the present investigation was to study the in vivo protective effect of eugenol against CCl4 toxicity. Eugenol (5 or 25 mg/kg body wt) given orally for 3 consecutive days did not alter the levels of serum glutamic oxalacetic transaminase (SGOT), microsomal enzymes such as cytochrome P450 reductase, glucose-6-phosphatase (G-6-Pase) xenobiotic-metabolizing enzymes (aminopyrine-N-demethylase, N-nitrosodimethylamine-demethylase and ethoxyresorufin-O-deethylase) and liver histology. Doses of eugenol (5 or 25 mg/kg) administered intragastrically to each rat on three consecutive days i.e. 48 hr, 24 hr and 30 min before a single oral dose of CCl4 (2.5 ml/kg body wt) prevented the rise in SGOT level without appreciable improvement in morphological changes in liver. Eugenol pretreatment also did not influence the decrease in microsomal cytochrome P450 content, G-6-Pase and xenobiotic-metabolizing enzymes brought about by CCl4. Since eugenol is metabolized and cleared rapidly from the body, the dose schedule was modified in another experiment. Eugenol (0.2, 1.0, 5.0 or 25 mg/kg) when given thrice orally i.e. prior to (-1 hr) along with (0 hr) and after (+3 hr) the i.p. administration of CCl4 (0.4 ml/kg) prevented significantly the rise in SGOT activity as well as liver necrosis. The protective effect was more evident at 1 mg and 5 mg eugenol doses. However, the decrease in microsomal G-6-Pase activity by CCl4 treatment was not prevented by eugenol suggesting that the damage to endoplasmic reticulum is not protected. The protective effect of eugenol against CCl4 induced hepatotoxicity is more evident when it is given concurrently or soon after rather than much before CCl4 treatment.