scholarly journals Protective Effects of Aqueous Extracts of Flos lonicerae Japonicae against Hydroquinone-Induced Toxicity in Hepatic L02 Cells

2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Yanfang Gao ◽  
Huanwen Tang ◽  
Liang Xiong ◽  
Lijun Zou ◽  
Wenjuan Dai ◽  
...  
Keyword(s):  
Dna Damage ◽  
Cell Viability ◽  
Dependent Manner ◽  
Aqueous Extracts ◽  
Protective Effects ◽  
Concentration Dependent Manner ◽  
Flos Lonicerae ◽  
L02 Cells ◽  
Flos Lonicerae Japonicae

Hydroquinone (HQ) is widely used in food stuffs and is an occupational and environmental pollutant. Although the hepatotoxicity of HQ has been demonstrated both in vitro and in vivo, the prevention of HQ-induced hepatotoxicity has yet to be elucidated. In this study, we focused on the intervention effect of aqueous extracts of Flos lonicerae Japonicae (FLJ) on HQ-induced cytotoxicity. We demonstrated that HQ reduced cell viability in a concentration-dependent manner by administering 160 μmol/L HQ for 12 h as the positive control of cytotoxicity. The aqueous FLJ extracts significantly increased cell viability and decreased LDH release, ALT, and AST in a concentration-dependent manner compared with the corresponding HQ-treated groups in hepatic L02 cells. This result indicated that aqueous FLJ extracts could protect the cytotoxicity induced by HQ. HQ increased intracellular MDA and LPO and decreased the activities of GSH, GSH-Px, and SOD in hepatic L02 cells. In addition, aqueous FLJ extracts significantly suppressed HQ-stimulated oxidative damage. Moreover, HQ promoted DNA double-strand breaks (DSBs) and the level of 8-hydroxy-2′-deoxyguanosine and apoptosis. However, aqueous FLJ extracts reversed HQ-induced DNA damage and apoptosis in a concentration-dependent manner. Overall, our results demonstrated that the toxicity of HQ was mediated by intracellular oxidative stress, which activated DNA damage and apoptosis. The findings also proved that aqueous FLJ extracts exerted protective effects against HQ-induced cytotoxicity in hepatic L02 cells.

scholarly journals Protective Effects of Extracts fromFructus rhodomyrtiagainst Oxidative DNA DamageIn VitroandIn Vivo

2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Yuebin Ke ◽  
Xinyun Xu ◽  
Shuang Wu ◽  
Juan Huang ◽  
Yijie Geng ◽  
...  
Keyword(s):  
Dna Damage ◽  
Oxidative Dna Damage ◽  
Antioxidant Properties ◽  
Dependent Manner ◽  
Protective Effects ◽  
Concentration Dependent Manner ◽  
Spleen Lymphocytes ◽  
Endogenous Antioxidant

Objective. To evaluate the potential protective effects of extracts fromFructus rhodomyrti(FR) against oxidative DNA damage using a cellular system and the antioxidant ability onpotassiumbromate- (KBrO3-) mediated oxidative stress in rats.Methods. The effects of FR on DNA damage induced by hydrogen peroxide (H2O2) were evaluated by comet assay in primary spleen lymphocytes cultures. The effects of FR on the activities of SOD, CAT, and GPx and the levels of GSH, hydroperoxides, and 8-OHdG were determined in the plasma and tissues of rats treated with KBrO3.Results. FR was shown to effectively protect against DNA damage induced by H2O2  in vitro, and the maximum protective effect was observed when FR was diluted 20 times. Endogenous antioxidant status, namely, the activities of SOD, CAT, and GPx and the levels of GSH were significantly decreased in the plasma, the liver, and the kidney of the KBrO3-treated rats, while the pretreatment of FR prevented the decreases of these parameters. In addition, the pretreatment of FR was also able to prevent KBrO3-induced increases in the levels of hydroperoxides and 8-OHdG in the plasma, the liver, and the kidney in rats.Conclusions. Our findings suggested that FR might act as a chemopreventive agent with antioxidant properties offering effective protection against oxidative DNA damage in a concentration-dependent mannerin vitroandin vivo.

Properties of neuroprotective cell-permeant Ca2+ chelators: effects on [Ca2+]i and glutamate neurotoxicity in vitro

1994 ◽  
Vol 72 (4) ◽  
pp. 1973-1992 ◽  
Author(s):  
M. Tymianski ◽  
M. P. Charlton ◽  
P. L. Carlen ◽  
C. H. Tator
Keyword(s):  
Time Course ◽  
Dependent Manner ◽  
Protective Effects ◽  
Tetraacetic Acid ◽  
Acetoxymethyl Ester ◽  
Neuroprotective Effects ◽  
Concentration Dependent Manner ◽  
Fura 2 ◽  
Glutamate Neurotoxicity

1. Cell-permeant Ca2+ chelators such as 1,2-bis-(2-amino-phenoxy)ethane- N,N,N',N'-tetraacetic acid acetoxymethyl ester (BAPTA-AM) protect neurons against excitotoxic and ischemic neuronal injury in vitro and in vivo. Here we provide the first steps toward characterizing the mechanisms by which these agents produce their neuroprotective effects. 2. Cultured mouse spinal neurons were simultaneously loaded with the Ca2+ indicator fura-2 and with one of three permeant chelators derived from the fast Ca2+ buffer BAPTA, or with ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid acetoxymethyl ester (EGTA-AM). Adding these chelators did not interfere with the fluorescence spectrum of fura-2 and had no effect on baseline [Ca2+]i. 3. The neurons were challenged with 250 microM L-glutamate for 50 min, producing a marked transient [Ca2+]i increase followed by a decay of [Ca2+]i to a lower “plateau.” About 80% of control neurons succumbed to this excitotoxic insult. Neurons that survived adjusted their plateau [Ca2+]i to lower levels than those that succumbed. 4. Neurons that were pretreated with permeant Ca2+ chelators became more resistant to these neurotoxic challenges. 5. We examined whether this reduction in glutamate neurotoxicity could be related to the given buffer's known Ca2+ affinity (Kd), its Ca2+ binding kinetics, and its ability to attenuate glutamate-induced [Ca2+]i increases. 6. Pretreatment of neurons with BAPTA analogues having Kds ranging from 100 to 3,600 microM 1) attenuated the amplitude and 2) lengthened the time constant describing the rise and decay of the glutamate-evoked [Ca2+]i transient. The magnitude of these effects paralleled the affinity of the chelator for Ca2+. 7. BAPTA-AM and its analogues dramatically attenuated the early neurotoxicity of glutamate, reducing cell deaths by up to 80%. However, in contrast with the graded effects of chelators having different Ca2+ affinities on Ca2+ transients, all BAPTA analogues were equally protective. These protective effects did not relate to the chelators' Ca2+ affinity within a Kd range of 100 nM (for BAPTA) to 3,600 nM (for 5,5'-dibromo BAPTA). 8. BAPTA-AM protected neurons in a concentration-dependent manner with 50% protection obtained with 10 microM, a concentration having no effect on the [Ca2+]i transient amplitude. 9. EGTA, a slow Ca2+ buffer with a similar Ca2+ affinity to BAPTA produced the same effects as BAPTA on [Ca2+]i transient kinetics. However, it was far less protective than BAPTA. 10. The time course of early glutamate neurotoxicity was altered by the BAPTA analogues, but not EGTA. BAPTA analogues caused a small increase in cell deaths in the first minutes of each experiment, followed by relative sparing from further neurodegeneration. 11. The ability of low Ca2+ affinity chelators such as 5,5'-dibromo BAPTA to protect neurons without markedly attenuating measured [Ca2+]i increases conflicts with the hypothesis that global elevations in [Ca2+]i are responsible for triggering neurotoxicity.(ABSTRACT TRUNCATED AT 400 WORDS)

Protective Effects on Mitochondria and Anti-Aging Activity of Polysaccharides from Cultivated Fruiting Bodies of Cordyceps militaris

2010 ◽  
Vol 38 (06) ◽  
pp. 1093-1106 ◽  
Author(s):  
Xing-Tai Li ◽  
Hong-Cheng Li ◽  
Chun-Bin Li ◽  
De-Qiang Dou ◽  
Ming-Bo Gao
Keyword(s):  
Hydroxyl Radicals ◽  
Cordyceps Militaris ◽  
Mitochondrial Swelling ◽  
Dependent Manner ◽  
Protective Effects ◽  
Fruiting Bodies ◽  
Concentration Dependent Manner ◽  
Mitochondrial Injury

Cordyceps militaris (L.) Link is an entomopathogenic fungus parasitic to Lepidoptera larvae, and is widely used as a folk tonic or invigorant for longevity in China. Although C. militaris has been used in traditional Chinese medicine for millennia, there is still a lack convincing evidence for its anti-aging activities. This study was performed to investigate the effects of polysaccharides from cultivated fruiting bodies of C. militaris (CMP) on mitochondrial injury, antioxidation and anti-aging activity. Fruiting bodies of C. militaris were cultivated artificially under optimized conditions. The spectrophotometric method was used to measure thiobarbituric acid reactive substances (TBARS), mitochondrial swelling, and activities of scavenging superoxide anions in vitro. D-galactose (100 mg/kg/day) was injected subcutaneously into back of the neck of mice for 7 weeks to induce an aging model. The effects of CMP on the activities of catalase (CAT), surperoxide dismutase (SOD), glutathione peroxidase (GPx) and anti-hydroxyl radicals were assayed in vivo using commercial monitoring kits. The results showed that CMP could inhibit mitochondrial injury and swelling induced by Fe2+ -L-Cysteine in a concentration- dependent manner and it also had a significant superoxide anion scavenging effect. Moreover, the activities of CAT, SOD, GPx and anti-hydroxyl radicals in mice liver were increased significantly by CMP. These results indicate that CMP protects mitochondria by scavenging reactive oxygen species (ROS), inhibiting mitochondrial swelling, and increasing the activities of antioxidases. Therefore, CMP may have pharmaceutical values for mitochondrial protection and anti-aging. CMP was the major bioactive component in C. militaris.

Dimethyloxalylglycine (DMOG) and the Caspase Inhibitor “Ac-LETD-CHO” Protect Neuronal ND7/23 Cells of Gluocotoxicity

2019 ◽  
Author(s):  
Debasmita Mukhopadhyay ◽  
Mohammad Hammami ◽  
Amani Khalouf ◽  
Yazan Al Shaikh ◽  
Abdul Khader Mohammed ◽  
...  
Keyword(s):  
Dna Damage ◽  
Cell Viability ◽  
Dependent Manner ◽  
Ros Production ◽  
Protective Effects ◽  
Caspase Inhibitor ◽  
Novel Therapy ◽  
Pharmacological Agents ◽  
Micro Rnas ◽  
The Impact

AbstractIt well known that long-lasting hyperglycaemia disrupts neuronal function and leads to neuropathy and other neurodegenerative diseases. The α-ketoglutarate analogue (DMOG) and the caspase-inhibitor “Ac-LETD-CHO are potential neuroprotective molecules. Whether their protections may also extend glucotoxicity-induced neuropathy is not known. Herein, we evaluated the possible cell-protective effects of DMOG and Ac-LETD-CHO against hyperglycaemia-induced reactive oxygen species and apoptosis in ND7/23 neuronal cells. The impact of glucotoxicity on the expression of HIF-1α and a panel of micro-RNAs of significance in hyperglycaemia and apoptosis was also investigated.ND7/23 cells cultured under hyperglycaemic conditions showed decreased cell viability and elevated levels of ROS production in a dose- and time-dependent manner. However, presence DMOG (500 µM) and/or Ac-LETD-CHO (50 µM) counteracted this effect and increase cell viability concomitant with reduction in ROS production, DNA damage and apoptosis. AcLETD-CHO suppressed hyperglycaemia-induced caspase 3 activation in ND7/23 cells. Both DMOG and Ac-LETD-CHO increased HIF-1α expression paralleled with the suppression of miR-126–5p, miR-128–3p and miR-181 expression and upregulation of miR-26b, 106a-5p, 106b-5p, 135a-5p, 135b-5p, 138–5p, 199a-5p, 200a-3p and 200c-3p expression.We demonstrate a mechanistic link for the DMOG and Ac-LETD-CHO protection against hyperglycaemia-induced neuronal dysfunction, DNA damage and apoptosis and thereby propose that pharmacological agents mimicking these effects may represent a promising novel therapy for the hyperglycaemia-induced neuropathy.

scholarly journals In Vitro Antioxidant Capacity and Neuronal Cell Toxicity of Roots of Ostericum koreanum Maximowicz

2011 ◽  
Vol 8 (3) ◽  
pp. 1451-1455
Author(s):  
Ramalingam Mahesh ◽  
Hyo Won Jung ◽  
Jun Hong Park ◽  
Yong-Ki Park
Keyword(s):  
Cell Viability ◽  
Ethyl Acetate ◽  
Antioxidant Activities ◽  
Radical Scavenging ◽  
Neuronal Cell ◽  
Ethyl Acetate Fraction ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Ostericum Koreanum

Ostericum koreanummaximowicz (Umbelliferae), a medicinal herb in Korean Oriental Medicine, has been applied to treat cold, headache, neuralgia and arthralgia. The ethyl acetate fraction ofO. koreanumroot was subjected toin vitroantioxidant activity with different methods for free radical scavenging activities. In addition, the cell viability and nitric oxide release assays were performed here for the first time in neuroblastoma (Neuro-2a) cell cultures. Among all the tested methods, the ethyl acetate fraction was expressed very active, exhibiting a good Trolox equivalent values and IC50, comparable to that of the commercial antioxidants, Trolox and ascorbic acid, respectively. The results showed that there was a reduction of cell viability by the fraction in a concentration dependent manner. These results suggest thatO. koreanumshows good antioxidant activitiesin vitroby inhibiting free radicals. These findings provide a rationale for thein vivotesting. Also, the major constituents behind the antioxidant mechanisms of this fraction warrant further study.

scholarly journals Atheroprotective action of a modified organoselenium compound: in vitro evidence

2016 ◽  
Vol 88 (3 suppl) ◽  
pp. 1953-1965 ◽  
Author(s):  
JADE DE OLIVEIRA ◽  
MARCOS R. STRALIOTTO ◽  
GIANNI MANCINI ◽  
CLAUDIA P. FIGUEIREDO ◽  
ANTÔNIO L. BRAGA ◽  
...  
Keyword(s):  
Foam Cell ◽  
Oxidized Ldl ◽  
Ldl Oxidation ◽  
Foam Cell Formation ◽  
Dependent Manner ◽  
Protective Effects ◽  
Organoselenium Compound ◽  
Organoselenium Compounds ◽  
Concentration Dependent Manner

ABSTRACT Oxidation of low-density lipoprotein (LDL) has been strongly suggested to play a significant role in the pathogenesis of atherosclerosis. Thus, reducing LDL oxidation is a potential approach to decrease the risk of the atherosclerosis. Organoselenium compounds have demonstrated promising atheroprotective properties in experimental models. Herein, we tested the in vitro atheroprotective capability of a modified organoselenium compound, Compound HBD, in protecting isolated LDL from oxidation as well as foam cells formation. Moreover, the glutathione peroxidase (GPx)-like activity of Compound HBD was analyzed in order to explore the mechanisms related to the above-mentioned protective effects. The Compound HBD in a concentration-dependent manner reduced the Cu2+-induced formation of conjugated dienes. The protein portion from LDL were also protected from Cu2+-induced oxidation. Furthermore, the Compound HBD efficiently decreased the foam cell formation in J774 macrophage cells exposed to oxidized LDL. We found that the atheroprotective effects of this compound can be, at least in part, related to its GPx-like activity. Our findings demonstrated an impressive effect of Compound HBD against LDL-induced toxicity, a further in vivo study to investigate in more detail the antioxidant and antiatherogenic effects of this compound could be considered.

Modifications of cellular responses to lysophosphatidic acid and platelet-activating factor by plasma gelsolin

2007 ◽  
Vol 292 (4) ◽  
pp. C1323-C1330 ◽  
Author(s):  
Teresia M. Osborn ◽  
Claes Dahlgren ◽  
John H. Hartwig ◽  
Thomas P. Stossel
Keyword(s):  
Platelet Activating Factor ◽  
Protective Role ◽  
Actin Binding ◽  
Dependent Manner ◽  
Protective Effects ◽  
Concentration Dependent Manner ◽  
Blood Concentrations ◽  
Plasma Gelsolin

Gelsolin is a highly conserved intracellular actin-binding protein with an extracellular isoform, plasma gelsolin (pGSN). Blood concentrations of pGSN decrease in response to diverse tissue injuries. Depletion of pGSN to critical levels precedes and often predicts complications of injuries such as lung permeability changes and death. Administration of recombinant pGSN ameliorates such complications and reduces mortality in animal models. One proposed mechanism for pGSN's protective effects is that it inhibits inflammatory mediators generated during primary injuries, since pGSN binds bioactive mediators, including lysophospatidic acid (LPA) and endotoxin in vitro. However, no direct evidence in support of this hypothesis has been available. Here we show that recombinant pGSN modestly inhibited LPA-induced P-selectin upregulation by human platelets in the presence of albumin ( P < 0.0001). However, physiologically relevant pGSN concentrations inhibit platelet-activating factor (PAF)-mediated P-selectin expression by up to 77% ( P < 0.0001). pGSN also markedly inhibited PAF-induced superoxide anion (O2−) production of human peripheral neutrophils (PMN) in a concentration-dependent manner ( P < 0.0001). A phospholipid-binding peptide derived from pGSN (QRLFQVKGRR) also inhibited PAF-mediated O2− generation ( P = 0.024). Therefore, pGSN interferes with PAF- and LPA-induced cellular activation in vitro, suggesting a mechanism for the protective role of pGSN in vivo.

scholarly journals Cytotoxic, genotoxic and apoptotic effects of Viburnum opulus on colon cancer cells: an in vitro study

2020 ◽  
Vol 0 (0) ◽  
Author(s):  
Kubra Bozali ◽  
Eray Metin Guler ◽  
Ahmet Sadik Gulgec ◽  
Abdurrahim Kocyigit
Keyword(s):  
Colorectal Cancer ◽  
Dna Damage ◽  
Cell Viability ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Methanolic Extract ◽  
Cancer Cell Line ◽  
Dependent Manner ◽  
Apoptotic Effects

AbstractObjectiveIntake of various fruits is quite significant for maintaining the human body, due to their supply of useful constituents. V. opulus has been found to have outstanding antioxidant activity while showing a pro-oxidant effect at high doses. Due to this feature, V. opulus would be anticipated to have a healing impact on cancer treatment. In this study, it has been proposed to examine the cytotoxic, genotoxic, and apoptotic effects of V. opulus on human colorectal cancer cell.MethodDifferent concentrations of V. opulus methanolic extract (5–2000 μg/mL) were incubated for 24 h with colorectal cancer cell line (Lovo). The cell viability, intracellular reactive oxygen species (iROS), DNA damage, and apoptosis were measured after incubation.ResultsThe obtained results of this research demonstrate decreased cell viability and increased DNA damage, iROS, and apoptosis levels of V. opulus in Lovo cells in a concentration-dependent manner in the range of 14.88–52.06%. There were strong positive relationships between apoptosis, genotoxicity, and cytotoxicity in V. opulus methanolic extract treated cancer cell line.DiscussionThis in vitro research clearly demonstrated that V. opulus methanolic extract induces DNA damage, apoptosis, and cytotoxicity in a dose-dependent manner in cancer cells due to its pro-oxidant activity.ConclusionAlthough in vitro results are favorable, in vivo and further studies are needed.

scholarly journals Investigation of Hepatoprotective and Antioxidant Activity of Celosia argentea against Tissue Injury Caused by Rifampicin Administration

2019 ◽  
pp. 1-11 ◽  
Author(s):  
Abiodun Olusoji Owoade ◽  
Adewale Adetutu ◽  
Olubukola Sinbad Olorunnisola ◽  
Olufemi Ogundeji Ogundipe
Keyword(s):  
Tissue Injury ◽  
Radical Scavenging ◽  
Hdl Cholesterol ◽  
Dependent Manner ◽  
Protective Effects ◽  
Sod Activity ◽  
Concentration Dependent Manner ◽  
Celosia Argentea ◽  
Liver And Kidney

This study evaluated the antioxidant and possible protective effects of Celosia argentea against tissue injury caused by rifampicin administration. The antioxidant property of the aqueous extract of C. argentea was assessed in-vitro using 2,2-Diphenyl-1- picrylhydrazyl (DPPH), and 2,2-azino-bis (3-ethylbenzthiazoline-6-sufonic acid) (ABTS) assays. The results obtained revealed the free radical scavenging ability of the extract against the radicals in a concentration-dependent manner. Administration of rifampicin to rats for 28 days induced a significant increase in the activities of alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), and increase cholesterol levels in the plasma, liver and kidney while HDL cholesterol was decreased. It also elevated the levels of malondialdehyde (MDA) and decreased superoxide dismutase (SOD) activities in the liver and kidney. However, co-administration of C. argentea extract to rifampicin treated rats significantly reversed all these rifampicin induced changes. The levels of AST, ALT, ALP and cholesterol in the plasma, liver and kidney were decreased while HDL cholesterol level was increased. In addition, SOD activity was elevated while MDA was depressed when compared to the rifampicin treated rats. The extract of C. argentea was found to be rich in phenolic content and was proved to have no toxic effects on rats when administered alone to normal rats at a dose level of 400mg/kg/day. This study demonstrated that C. argentea leaf extract ameliorates rifampicin-induced hepatotoxicity and could be exploited in the management of hepatotoxic effect associated with rifampicin treatment.

scholarly journals Baicalein inhibits cell development in papillary thyroid cancer by regulating miR-206/RAP1B pathway

2020 ◽  
Vol 19 (7) ◽  
pp. 1383-1388 ◽  
Author(s):  
Peng Wang ◽  
Liang Guo ◽  
Zhong Liang ◽  
Jianlin Lou ◽  
Jianqiang Zhao
Keyword(s):  
Thyroid Cancer ◽  
Cell Viability ◽  
Papillary Thyroid Cancer ◽  
Migration And Invasion ◽  
Dependent Manner ◽  
Papillary Thyroid ◽  
Concentration Dependent Manner ◽  
And Control ◽  
Interfering Rna

Purpose: To investigate the therapeutic effect of baicalein on papillary thyroid cancer (PTC) cells in vitro and its underlying molecular mechanism.Methods: The human PTC cell line TPC-1 was divided into five groups and treated with distilled water or baicalein at 10, 20, 50, or 100 μM. Next, miR-206, miR-206 inhibitor, the respective negative controls of miR-206 and miR-206 inhibitor, RAP1B small interfering RNA (siRNA), and control vector siRNA were synthesized and transfected into TPC-1 cells. Cell viability, migration, and invasion were measured using the 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) and Transwell assays. miR-206 expression and Ras-related protein (RAP1B) levels were assessed by quantitative real-time reverse transcription-polymerase chain reaction and western blotting, respectively.Results: Baicalein inhibited TPC-1 cell viability, migration and invasion, upregulated miR-206 expression, and reduced the RAP1B level in a concentration-dependent manner (p < 0.01). miR-206 negatively regulated RAP1B expression and increased the baicalein-induced reduction of RAP1B expression. Moreover, RAP1B overexpression relieved the suppression of cell viability, migration, and invasion caused by baicalein (p < 0.01).Conclusion: Baicalein suppresses cell growth in PTC cells by regulating the miR-206/RAP1B pathway, providing a new therapeutic strategy for PTC treatment. Keywords: Baicalein, Papillary thyroid cancer (PTC), miR-206, RAP1B, Cell viability, Cell invasion

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