Potential beneficial effect of naringenin on lipid peroxidation and antioxidant status in rats with ethanol-induced hepatotoxicity

Jayaraman, Jayachitra; Veerappan, Muniappan; Nalini, Namasivayam

doi:10.1211/jpp.61.10.0016

Cited by 48 publications

(24 citation statements)

References 51 publications

(51 reference statements)

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“…On the other hand, BREE (125 and 250 mg/kg bw) treated groups significantly (P≤0.05) alleviate the TBA, SOD, GSH and F2-isoprostanes to near normal levels (Table 4). This decrease could be due to ROS inefficient scavenging which might be implicated to oxidative inactivation of enzymes (Jayaraman et al, 2009), which proves to be a potent antioxidant, a finding that correlates with recent reports Arulmozhi et al, 2012;Hsieh et al, 2008). Furthermore, the antioxidant property and the oxygen-radical scavenger of the extract may therefore be due to the presence of polyphenolic high content compounds such as anthocyanins and flavonoids (Mira et al, 2009;Yawadio et al, 2007;Zhang et al, 2010).…”

Section: Effect Of Bree On Tba Sod Gsh and F2-isoprostanes Activitisupporting

confidence: 68%

Preventive effect of black rice antioxidant extract on oxidative stress induced by ethyl alcohol

Al-Jameel¹,

El-Rahman²

2018

Afr. J. Biotechnol.

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The present study investigated the black rice ethanolic extract (BREE) protective effect as natural antioxidants against oxidative stress induced by ethyl alcoholic (EA) in male rats. BREE flavonoids and phenols were determined by high performance liquid chromatography (HPLC). The study was conducted on 40 male Wistar rats weighing 170±2 g, the animals divided into 4 equal groups. The first group was given distilled water (DW) and used as a negative control (NC) group. The second group was administrated EA (6 g/kg bw/day) and used as positive control (PC) group. The other groups of rats were administrated [BREE 125 or 250 mg/kg bw + EA 6 g/kg bw/day]. Blood samples were collected after 10 days. Lipid profile, thiobarbituric acid (TBA), superoxide dismutase (SOD), glutathione (GSH) and F2-isoprostanes (F2-isoPs) were determined. The results indicate that the rats treated with EA 6 g/kg bw/day showed a significant (p≤0.05) increase in the levels of total cholesterol (TC), low density lipoprotein-cholesterol (LDL-C), TBA and F2-isoprostanes and significant (p≤0.05) decrease in highdensity lipoprotein-cholesterol (HDL-C), SOD and GSH levels. The rise in serum TC, LDL-C, TBA and F2-isoprostanes were significantly attenuated by BREE 125 or 250 mg/kg bw + EA 6 g/kg bw/day. Also, the levels of serum HDL-C, SOD and GSH in BREE 125 or 250 mg/kg bw + EA 6 g/kg bw/day groups showed a significant (p≤0.05) increase as compared to PC group. The current results ascertained the beneficial effects of BREE in controlling oxidative stress induced by ethyl alcohol in male rats.

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Section: Effect Of Bree On Tba Sod Gsh and F2-isoprostanes Activitisupporting

confidence: 68%

Preventive effect of black rice antioxidant extract on oxidative stress induced by ethyl alcohol

Al-Jameel¹,

El-Rahman²

2018

Afr. J. Biotechnol.

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“…NAR was able to prevent LPO due to its molecular structure; perhaps its hydroxyl groups facilitate its adherence to lipid bilayer polar groups, and its nonpolar nucleus may interact with hydrophobic tails of phospholipids, thereby reducing the deleterious effects of free radicals on membranes[12,42,43]. …”

Section: Discussionmentioning

confidence: 99%

Naringenin prevents experimental liver fibrosis by blocking TGFβ-Smad3 and JNK-Smad3 pathways

Hernández-Aquino

Zarco

Casas‐Grajales

et al. 2017

WJG

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AIMTo study the molecular mechanisms involved in the hepatoprotective effects of naringenin (NAR) on carbon tetrachloride (CCl4)-induced liver fibrosis.METHODSThirty-two male Wistar rats (120-150 g) were randomly divided into four groups: (1) a control group (n = 8) that received 0.7% carboxy methyl-cellulose (NAR vehicle) 1 mL/daily p.o.; (2) a CCl4 group (n = 8) that received 400 mg of CCl4/kg body weight i.p. 3 times a week for 8 wk; (3) a CCl4 + NAR (n = 8) group that received 400 mg of CCl4/kg body weight i.p. 3 times a week for 8 wk and 100 mg of NAR/kg body weight daily for 8 wk p.o.; and (4) an NAR group (n = 8) that received 100 mg of NAR/kg body weight daily for 8 wk p.o. After the experimental period, animals were sacrificed under ketamine and xylazine anesthesia. Liver damage markers such as alanine aminotransferase (ALT), alkaline phosphatase (AP), γ-glutamyl transpeptidase (γ-GTP), reduced glutathione (GSH), glycogen content, lipid peroxidation (LPO) and collagen content were measured. The enzymatic activity of glutathione peroxidase (GPx) was assessed. Liver histopathology was performed utilizing Masson’s trichrome and hematoxylin-eosin stains. Zymography assays for MMP-9 and MMP-2 were carried out. Hepatic TGF-β, α-SMA, CTGF, Col-I, MMP-13, NF-κB, IL-1, IL-10, Smad7, Smad3, pSmad3 and pJNK proteins were detected via western blot.RESULTSNAR administration prevented increases in ALT, AP, γ-GTP, and GPx enzymatic activity; depletion of GSH and glycogen; and increases in LPO and collagen produced by chronic CCl4 intoxication (P < 0.05). Liver histopathology showed a decrease in collagen deposition when rats received NAR in addition to CCl4. Although zymography assays showed that CCl4 produced an increase in MMP-9 and MMP-2 gelatinase activity; interestingly, NAR administration was associated with normal MMP-9 and MMP-2 activity (P < 0.05). The anti-inflammatory, antinecrotic and antifibrotic effects of NAR may be attributed to its ability to prevent NF-κB activation and the subsequent production of IL-1 and IL-10 (P < 0.05). NAR completely prevented the increase in TGF-β, α-SMA, CTGF, Col-1, and MMP-13 proteins compared with the CCl4-treated group (P < 0.05). NAR prevented Smad3 phosphorylation in the linker region by JNK since this flavonoid blocked this kinase (P < 0.05).CONCLUSIONNAR prevents CCl4 induced liver inflammation, necrosis and fibrosis, due to its antioxidant capacity as a free radical inhibitor and by inhibiting the NF-κB, TGF-β-Smad3 and JNK-Smad3 pathways.

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“…Previous studies have demonstrated that naringenin exhibits various pharmacological effects, including anti-tumor, anti-mutagenic and anti-atherosclerotic effects (17)(18)(19). Studies have suggested that naringenin may reverse the liver damage caused by drugs or toxic chemical compounds, including alcohol, cadmium, carbon tetrachloride, oxytetracycline and dimethyl nitrosamine (20)(21)(22)(23). The present study aimed to investigate the effects of naringenin on DACD.…”

Section: Introductionmentioning

confidence: 96%

Naringin ameliorates cognitive deficits via oxidative stress, proinflammatory factors and the PPARγ signaling pathway in a type 2 diabetic rat model

Liang

et al. 2015

Molecular Medicine Reports

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Naringenin is a flavonoid polyphenolic compound, which facilitates the removal of free radicals, oxidative stress and inflammation. The present study aimed to obtain a better understanding of the effects of curcumin on the regulation of diabetes‑associated cognitive decline, and its underlying mechanisms. An experimental diabetes mellitus (DM) rat model was induced by streptozoticin (50 mg/kg). Following treatment with naringin (100 and 200 mg/kg) for 16 weeks, the body weight and blood glucose levels of the DM rats were measured. A morris water maze test was used to analyze the effects of naringin on the cognitive deficit of the DM rats. The levels of oxidative stress, proinflammatory factors, caspase‑3 and caspase‑9, and the protein expression of peroxisome proliferator‑activated receptor γ (PPARγ) were quantified in the DM rats using a commercially‑available kit and western blot assay, respectively. In addition, a GW9662 PPARγ inhibitor (0.3 mg/kg) was administered to the DM rats to determine whether PPARγ affected the effects of naringin on the cognitive deficit of the DM rats. The results demonstrated that naringin increased the body weight, blood glucose levels, and cognitive deficits of the DM rats. The levels of oxidative stress and proinflammatory factors in the naringin‑treated rats were significantly lower, compared with those of the DM rats. In addition, naringin activated the protein expression of PPARγ, and administration of the PPARγ inhibitor decreased the protein expression of PPARγ, and attenuated the effects of naringin on cognitive deficit. The results also demonstrated that naringin decreased the expression levels of caspase‑3 and caspase‑9 in the DM rats. These results suggested that naringin ameliorated cognitive deficits via oxidative stress, proinflammatory factors and the PPARγ signaling pathway in the type 2 diabetic rat model. Furthermore, oxidative stress, proinflammatory factors and PPARγ signaling may be involved in mediating these effects.

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Potential beneficial effect of naringenin on lipid peroxidation and antioxidant status in rats with ethanol-induced hepatotoxicity

Abstract: Taken together these findings suggest that naringenin has a therapeutic potential in the abatement of ethanol-induced hepatotoxicity.

Cited by 48 publications

References 51 publications

Preventive effect of black rice antioxidant extract on oxidative stress induced by ethyl alcohol

Preventive effect of black rice antioxidant extract on oxidative stress induced by ethyl alcohol

Naringenin prevents experimental liver fibrosis by blocking TGFβ-Smad3 and JNK-Smad3 pathways

Naringin ameliorates cognitive deficits via oxidative stress, proinflammatory factors and the PPARγ signaling pathway in a type 2 diabetic rat model

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