scholarly journals Nanoencapsulation of Curcumin and Its Protective Effects against CCl4-Induced Hepatotoxicity in Mice

2019 ◽  
Vol 2019 ◽  
pp. 1-10 ◽  
Author(s):  
Jian Li ◽  
Ruixu Niu ◽  
Lixin Dong ◽  
Liming Gao ◽  
Jie Zhang ◽  
...  
Keyword(s):  
Liver Injury ◽  
Acute Liver Injury ◽  
Curcuma Longa ◽  
Stress Factors ◽  
Hepatoprotective Effect ◽  
Control Group ◽  
Antioxidant Enzyme Activities ◽  
Protective Effects ◽  
Model Control ◽  
Model Control Group

Curcumin is a natural phenolic compound extracted from the herb Curcuma longa L. rhizome and has received much attention on account of its biological properties. However, its poor solubility and low bioavailability limit its use. The purpose of this study was to synthesize curcumin-loaded nanoliposomes (Cur-NLs) to improve their bioavailability and evaluate the hepatoprotective effect of Cur-NLs against tetrachloromethane- (CCl4-) induced acute liver injury in mice. We prepared Cur-NLs by thin film dispersion method, and the characterizations of Cur-NLs were measured by transmission microscope, laser particle size analyzer, infrared spectrometer, and X-ray diffraction. After 14 days pretreatment of Cur-NLs, free curcumin, silybin, or PBS, the models of acute liver injury were established by CCl4 intraperitoneal injection in mice. The organ index, biochemical liver function parameters, histopathology, and antioxidant enzyme activities of liver tissues were measured further to evaluate the protective effects of Cur-NLs on liver injury. Compared with the CCl4 model control group, pretreatment of Cur-NLs effectively reduced the serum levels of ALT, AST, and ALP and attenuated the hepatic necrosis induced by CCl4 intoxication. Furthermore, Cur-NL pretreatment remarkably exhibited decreased MDA level and increased SOD, GPx, and CAT activities compared to CCl4 model control group. Compared with the free curcumin group, the Cur-NLs also showed a better hepatoprotective effect. These observations imply that Cur-NLs act as a promising hepatoprotective agent in reducing liver oxidative stress produced by different stress factors.

scholarly journals Cardamonin Reduces Acetaminophen-Induced Acute Liver Injury in Mice via Activating Autophagy and NFE2L2 Signaling

2020 ◽  
Vol 11 ◽  
Author(s):  
Qiushi Xu ◽  
Yunhui Fan ◽  
Juan J. Loor ◽  
Yusheng Liang ◽  
Xudong Sun ◽  
...  
Keyword(s):  
Liver Injury ◽  
Acute Liver Injury ◽  
High Mobility ◽  
Hepatoprotective Effect ◽  
Receptor Protein ◽  
Related Factor ◽  
Protective Effects ◽  
Toll Like Receptor 4 ◽  
Sequestosome 1 ◽  
Underlying Mechanisms

Cardamonin (CD), a naturally occurring chalcone derived from the Alpinia species, has been shown to exert antioxidant and anti-inflammatory activity, but its role in the prevention of acetaminophen- (APAP-) induced hepatotoxicity remains elusive. The objective of this study was to determine the protective effects of CD against APAP-induced acute liver injury (ALI) and the underlying mechanisms. Wild-type or transcription factor nuclear factor erythroid 2-related factor 2- (NFE2L2-) deficient mice were treated with CD (50 or 100 mg/kg, i.p.) or vehicle for 24 h. Subsequently, these mice were challenged with APAP (400 mg/kg, i.p.) for 6 h. Liver and blood samples were collected to evaluate liver injury and protein abundance. Treatment with CD significantly reduced APAP-induced hepatotoxicity. Furthermore, CD effectively reduced APAP-induced inflammation by inhibiting high mobility group box 1 (HMGB1), toll-like receptor 4 (TLR4), and NOD-like receptor protein 3 (NLRP3) signaling. In addition, CD induced activation of sequestosome 1 (p62) and NFE2L2 signaling and facilitated autophagy. By applying autophagy inhibitor 3-methyladenine (3-MA; 20 mg/kg, i.p.), further mechanistic exploration revealed that NFE2L2 deficiency promoted autophagic activity induced by CD treatment, which was conducive to the hepatoprotective effect of CD against APAP-induced hepatoxicity in NFE2L2−/− mice. Overall, data suggest that CD has hepatoprotective effect against APAP-induced ALI, which might contribute to the activation of NFE2L2 and autophagy.

scholarly journals Protective Effects ofSalvia miltiorrhizaeon Multiple Organs of Rats with Obstructive Jaundice

2009 ◽  
Vol 2009 ◽  
pp. 1-9 ◽  
Author(s):  
Zhang Ling ◽  
Zhang Xiping ◽  
Qiu Fengmei ◽  
Yan Ping ◽  
Cheng Qihui
Keyword(s):  
Obstructive Jaundice ◽  
Treated Group ◽  
Control Group ◽  
Group Model ◽  
Protective Effects ◽  
Multiple Organs ◽  
Model Control ◽  
Model Control Group ◽  
Salvia Miltiorrhizae ◽  
The Impact

Purpose. we aim to explore the protective effects ofSalvia miltiorrhizaeinjection on multiple organs of obstructive jaundice (OJ) rats through observing the impact of this injection on the pathological alterations in these organs and the contents of endotoxin,PLA2, and TNF-αin the blood.Methods. A total of 90 mice were randomly divided into sham-operated group, model-control group, andSalvia miltiorrhizae-treated group (n=30). According to the duration of postoperative administration, each group was further divided into two subgroups, namely, 21 d subgroup (consecutive administration for 21 d,n=15) and 28 d subgroup (consecutive administration for 28 d,n=15). After administration, the pathological alterations in multiple organs were observed and the contents of endotoxin,PLA2, and TNF-αin the blood were determined.Results. Compared to model control group, the number of dead rats in treated group decreased though there was no statistical difference between the two groups. The pathological alterations in the liver, kidney, and spleen in treated group showed varying degrees of mitigation. At all time points, the contents of plasma endotoxin declined significantly. On day 28, plasmaPLA2content in treated group was significantly lower than that in model-control group.Conclusion.Salvia miltiorrhizaeinjection is able to obviously reduce the contents of inflammatory mediators in the blood of OJ rats and exert some protective effects on multiple organs of these rats.

scholarly journals Protective effects and mechanisms of microRNA-182 on oxidative stress in RHiN

2019 ◽  
Vol 14 (1) ◽  
pp. 400-409
Author(s):  
Lihua Li ◽  
Wenna Peng ◽  
Xiangrong Tian
Keyword(s):  
Oxidative Stress ◽  
Superoxide Dismutase ◽  
Survival Rate ◽  
Control Group ◽  
Mrna Levels ◽  
Protective Effects ◽  
Apoptosis Rate ◽  
Model Control ◽  
Model Control Group ◽  
Phosphoinositide 3 Kinase

AbstractTo explore protective effects and related mechanisms of microRNA-182 (miR-182) on oxidative stress in rat hippocampal neurons (RHiN), RHiN cells. As the results, the survival rate and superoxide dismutase levels in H2O2 group were significantly lower than H2O2+miR-182 group (all P<0.05). The malondialdehyde levels and apoptosis rate in H2O2+miR-182 group were significantly lower than H2O2 group (all P<0.05). The mRNA levels and expression levels of mTOR and PI3K in H2O2+miR-182 group were higher than those in H2O2 group (both P<0.05). The experiment of cerebral ischemic oxidative stress model rats showed that the survival rate, apoptosis rate, malondialdehyde and superoxide dismutase levels in miR-182 group were better than model control group. The positive staining intensity of phosphoinositide 3-kinase (mTOR) and phosphoinositide 3-kinase (PI3K) in model control group were significantly lower than miR-182 group (all P<0.05). Increased levels of miR-182 can reduce the damage of H2O2 treatments in RHiN cells. Oxidative stress is decreased in the neuronal cells possibly by activation of the PI3K-AKT-mTOR pathway.

scholarly journals Protective Effect and Mechanisms of Radix Astragali Injection on the Intestinal Mucosa of Rats with Obstructive Jaundice

2010 ◽  
Vol 2010 ◽  
pp. 1-8 ◽  
Author(s):  
Zhang Xiping ◽  
Weng Ke ◽  
Yu Yaping ◽  
Zhao Hongchan ◽  
Cheng Qihui
Keyword(s):  
Obstructive Jaundice ◽  
Intestinal Mucosa ◽  
Treated Group ◽  
Control Group ◽  
Protective Effects ◽  
Radix Astragali ◽  
Pathological Changes ◽  
Bax Protein ◽  
Model Control ◽  
Model Control Group

Objective. To research the protective effects and mechanisms of Radix Astragali injection on the intestinal mucosa of rats with obstructive jaundice (OJ).Methods. The rats were randomly divided into sham-operated, model control and Radix Astragali treated group. We observed the pathological changes of intestinal mucosa, expression levels of Bax and NF-κB proteins, and apoptosis indexes in intestinal mucosa as well as serum NO, MDA and SOD contents, respectively, on 7d, 14d, 21d and 28d after operation.Results. The pathological severity score (on 7d and 14d), apoptotic indexes (on 14d) of the intestinal mucosa and serum MDA content (on 14d) of treated group were significantly lower than those in the model control group (P<.05). The serum SOD contents (on all time points) of treated group were significantly higher than those in the model control group (P<.05). The sham-operated group (on 21d) of the product of staining intensity and positive rate of Bax protein was significantly lower than model control group (P<.05).Conclusion. Radix Astragali injection could protect the intestinal mucosa of OJ rats by increasing the content of SOD, reducing the content of MDA, inhibiting the apoptosis and relieving the pathological changes of intestinal mucosa.

scholarly journals Lemon Balm and Dandelion Leaf Extracts Synergistically Protect against Carbon Tetrachloride-Induced Acute Liver Injury in Mice

2021 ◽  
Vol 11 (1) ◽  
pp. 390
Author(s):  
Beom-Rak Choi ◽  
Il-Je Cho ◽  
Su-Jin Jung ◽  
Jae-Kwang Kim ◽  
Dae-Geon Lee ◽  
...  
Keyword(s):  
Carbon Tetrachloride ◽  
Liver Injury ◽  
Acute Liver Injury ◽  
Antioxidant Activities ◽  
Body Weight Gain ◽  
Histopathological Analysis ◽  
Related Factor ◽  
Mrna Levels ◽  
Protective Effects ◽  
Lemon Balm

Lemon balm and dandelion are commonly used medicinal herbs exhibiting numerous pharmacological activities that are beneficial for human health. In this study, we explored the protective effects of a 2:1 (w/w) mixture of lemon balm and dandelion extracts (MLD) on carbon tetrachloride (CCl4)-induced acute liver injury in mice. CCl4 (0.5 mL/kg; i.p.) injection inhibited body weight gain and increased relative liver weight. Pre-administration of MLD (50–200 mg/kg) for 7 days prevented these CCl4-mediated changes. In addition, histopathological analysis revealed that MLD synergistically alleviated CCl4-mediated hepatocyte degeneration and infiltration of inflammatory cells. MLD decreased serum aspartate aminotransferase and alanine transferase activities and reduced the number of liver cells that stained positive for cleaved caspase-3 and cleaved poly(ADP-ribose) polymerase, suggesting that MLD protects against CCl4-induced hepatic damage via the inhibition of apoptosis. Moreover, MLD attenuated CCl4-mediated lipid peroxidation and protein nitrosylation by restoring impaired hepatic nuclear factor erythroid 2-related factor 2 mRNA levels and its dependent antioxidant activities. Furthermore, MLD synergistically decreased mRNA and protein levels of tumor necrosis factor-α, interleukin-1β, and interleukin-6 in the liver. Together, these results suggest that MLD has potential for preventing acute liver injury by inhibiting apoptosis, oxidative stress, and inflammation.

scholarly journals Hepatoprotective effect of galangin on carbon tetrachloride-induced hepatotoxicity via the LKB1/AMPK pathway

2021 ◽  
Vol 19 ◽  
pp. 205873922110008
Author(s):  
Meng Chen ◽  
Xinyan Song ◽  
Jifang Jiang ◽  
Lei Xing ◽  
Pengfei Wang
Keyword(s):  
Carbon Tetrachloride ◽  
Liver Toxicity ◽  
Corn Oil ◽  
Histopathological Examination ◽  
Hepatoprotective Effect ◽  
Control Group ◽  
Group Model ◽  
Protective Effects ◽  
Model Group ◽  
Expression Levels

To investigate the protective effects of galangin on liver toxicity induced by carbon tetrachloride (CCl4) in mice. Mouse hepatotoxicity model was established by intraperitoneal injection (i.p.) of 10 ml/kg body weight CCl4 that diluted with corn oil to a proportion of 1:500 on Kunming mice. The mice were randomly divided into five groups named control group, model group, and 1, 5, and 10 mg/kg galangin group. The levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were analyzed by ELISA. Liver histopathological examination was observed via optical microscopy. The levels of superoxide dismutase (SOD), malondialdehyde (MDA), glutathione (GSH), and glutathion (GSSG) were analyzed to assess oxidative stress. Finally, western blot assay was carried out to analyse the expression levels of total AMP-activated protein kinase (AMPK), phospho-AMPK (p-AMPK), total liver kinase B1 (LKB1), and phospho-LKB1 (p-LKB1). Compared with the control group, in the model group, the levels of AST, ALT, MDA, and GSSG increased significantly ( p < 0.01); the activity of SOD and GSH decreased significantly ( p < 0.01); and the histopathological examination revealed liver necrosis. However, treatment with galangin (5 and 10 mg/kg) significantly reversed these CCl4-induced liver damage indicators. Furthermore, treatment with galangin (10 mg/kg) significantly increased the p-AMPK and p-LKB1 expression levels ( p < 0.01). This study supports the hepatoprotective effect of galangin against hepatotoxicity, perhaps occurring mainly through the LKB1/AMPK-mediated pathway.

scholarly journals Neurological Alterations and Testicular Damages in Aging Induced by D-Galactose and Neuro and Testicular Protective Effects of Combinations of Chitosan Nanoparticles, Resveratrol and Quercetin in Male Mice

Coatings ◽  
2021 ◽  
Vol 11 (4) ◽  
pp. 435
Author(s):  
Reham Z. Hamza ◽  
Mohammad S. Al-Harbi ◽  
Munirah A. Al-Hazaa
Keyword(s):  
Oxidative Stress ◽  
Chitosan Nanoparticles ◽  
Oxidative Stress Marker ◽  
Control Group ◽  
Antioxidant Enzyme Activities ◽  
Enzymatic Antioxidants ◽  
Protective Effects ◽  
Biochemical Alterations ◽  
Wide Range ◽  
Neurological Alterations

Aging is a neurological disease that is afforded by incidence of oxidative stress. Chitosan has received global interests due to its wide medical uses. Quercetin (Q) is a bioflavonoid and widely distributed in vegetables and fruits. Resveratrol is considered as a potent antioxidant and is a component of a wide range of foods. The using of either chitosan nanopartciles (CH-NPs), querectin (Q), and resveratrol (RV) to reduce the oxidative stress and biochemical alterations on brain and testicular tissues induced by D-galactose (DG) (100 mg/Kg) were the aim of the present study. This study investigated the probable protective effects of CH-NPs in two doses (140,280 mg/Kg), Q (20 mg/Kg) and RV (20 mg/Kg), against DG induced aging and neurological alterations. Brain antioxidant capacity as malonaldehyde (MDA), catalase (CAT), and glutathione reductase (GRx), as well as histopathological damages of the brain and testicular tissues were measured. The DG treated group had significantly elevated the oxidative stress markers by 96% and 91.4% in brain and testicular tissues respectively and lower significantly the antioxidant enzyme activities of both brain and testicular tissues than those of the control group by 86.95%, 69.27%, 83.07%, and 69.43%. Groups of DG that treated with a combination of CH-NPs in two doses, Q and RV, the levels of oxidative stress marker declined significantly by 68.70%, 76.64% in brain tissues and by 74.07% and 76.61% in testicular tissues, and the enzymatic antioxidants increased significantly by 75.55%, 79.24%, 62.32%, and 61.97% as compared to the DG group. The present results indicate that CH-NPs, Q, and RV have protective effects against DG-induced brain and testis tissue damage at the biochemical and histopathological levels. Mechanisms of this protective effect of used compounds against neurological and testicular toxicity may be due to the enhanced brain and testis antioxidant capacities.

scholarly journals Fucosterol Protects against Concanavalin A-Induced Acute Liver Injury: Focus on P38 MAPK/NF-κB Pathway Activity

2018 ◽  
Vol 2018 ◽  
pp. 1-13 ◽  
Author(s):  
Wenhui Mo ◽  
Chengfen Wang ◽  
Jingjing Li ◽  
Kan Chen ◽  
Yujing Xia ◽  
...  
Keyword(s):  
Liver Injury ◽  
P38 Mapk ◽  
Concanavalin A ◽  
Molecular Mechanisms ◽  
Therapeutic Agent ◽  
Acute Liver Injury ◽  
Biological Activities ◽  
Hepatic Necrosis ◽  
Protective Effects ◽  
Eisenia Bicyclis

Objective. Fucosterol is derived from the brown alga Eisenia bicyclis and has various biological activities, including antioxidant, anticancer, and antidiabetic properties. The aim of this study was to investigate the protective effects of fucosterol pretreatment on Concanavalin A- (ConA-) induced acute liver injury in mice, and to understand its molecular mechanisms. Materials and Methods. Acute liver injury was induced in BALB/c mice by ConA (25 mg/kg), and fucosterol (dissolved in 2% DMSO) was orally administered daily at doses of 25, 50, and 100 mg/kg. The levels of hepatic necrosis, apoptosis, and autophagy associated with inflammatory cytokines were measured at 2, 8, and 24 h. Results. Fucosterol attenuated serum liver enzyme levels and hepatic necrosis and apoptosis induced by TNF-α, IL-6, and IL-1β. Fucosterol also inhibited apoptosis and autophagy by upregulating Bcl-2, which decreased levels of functional Bax and Beclin-1. Furthermore, reduced P38 MAPK and NF-κB signaling were accompanied by PPARγ activation. Conclusion. This study showed that fucosterol could alleviate acute liver injury induced by ConA by inhibiting P38 MAPK/PPARγ/NF-κB signaling. These findings highlight that fucosterol is a promising potential therapeutic agent for acute liver injury.

scholarly journals Mechanism of KLF4 Protection against Acute Liver Injury via Inhibition of Apelin Signaling

2019 ◽  
Vol 2019 ◽  
pp. 1-10 ◽  
Author(s):  
Weitao Ji ◽  
Hongyun Shi ◽  
Hailin Shen ◽  
Jing Kong ◽  
Jiayi Song ◽  
...  
Keyword(s):  
Liver Injury ◽  
Signaling Pathway ◽  
Acute Liver Injury ◽  
Control Group ◽  
Necrosis Factor Alpha ◽  
Protein Levels ◽  
Klf4 Expression ◽  
Mrna And Protein Expression

Krüppel-like factor 4 (KLF4) is a key transcription factor that regulates genes involved in the proliferation or differentiation in different tissues. Apelin plays roles in cardiovascular functions, metabolic disease, and homeostatic disorder. However, the biological function of apelin in liver disease is still ongoing. In this study, we investigated the mechanism of KLF4-mediated protection against acute liver injury via the inhibition of the apelin signaling pathway. Mice were intraperitoneally injected with carbon tetrachloride (CCl4; 0.2 mL dissolved in 100 mL olive oil, 10 mL/kg) to establish an acute liver injury model. A KLF4 expression plasmid was injected through the tail vein 48 h before CCl4 treatment. In cultured LX-2 cells, pAd-KLF4 or siRNA KLF4 was overexpressed or knockdown, and the mRNA and protein levels of apelin were determined. The results showed that the apelin serum level in the CCl4-injected group was higher than that of control group, and the expression of apelin in the liver tissues was elevated while KLF4 expression was decreased in the CCl4-injected group compared to the KLF4-plasmid-injected group. HE staining revealed serious hepatocellular steatosis in the CCl4-injected mice, and KLF4 alleviated this steatosis in the mice injected with KLF4 plasmid. In vitro experiments showed that tumor necrosis factor-alpha (TNF-α) could downregulate the transcription and translation levels of apelin in LX-2 cells and also upregulate KLF4 mRNA and protein expression. RT-PCR and Western blotting showed that the overexpression of KLF4 markedly decreased basal apelin expression, but knockdown of KLF4 restored apelin expression in TNF-α-treated LX-2 cells. These in vivo and in vitro experiments suggest that KLF4 plays a key role in inhibiting hepatocellular steatosis in acute liver injury, and that its mechanism might be the inhibition of the apelin signaling pathway.

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