Modulation of oxidative stress response by flaxseed oil: Role of lipid peroxidation and underlying mechanisms

Yadav, Rajnish Kumar; Singh, Manjari; Roy, Subhadeep; Ansari, Mohd Nazam; Saeedan, Abdulaziz S.; Kaithwas, Gaurav

doi:10.1016/j.prostaglandins.2018.02.003

Cited by 54 publications

(28 citation statements)

References 56 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Previous published literature in vitro and in vivo studies suggested the anticancer effect of GLA. GLA reduced tumor growth in a WBC256 rat model; it also inhibited the cell growth of various rat carcinogenesis cell lines and human neuroblastoma cell lines 19,20. GLA treatment down-regulated mammary gland carcinogenesis and tumor growth.…”

Section: Introductionmentioning

confidence: 91%

Gamma linolic acid regulates PHD2 mediated hypoxia and mitochondrial apoptosis in DEN induced Hepatocellular carcinoma

Cui

Han

Zhang

et al. 2018

DDDT

View full text Add to dashboard Cite

IntroductionHepatocellular carcinoma (HCC) is one of the known major health problems across the globe, and is sixth ranked among all cancer, due to its high mortality rate. Polyunsaturated fatty acids (PUFAs) play an important role in the formation of a cell membrane, along with the fluidity of the membrane and proteins. Gamma linolenic acid (GLA) is member of the ω-6 family of PUFAs and converts into the arachidonic acid via a series of elongation and desaturation reactions. The aim of the current investigation was to scrutinize the effect of GLA on mitochondrial mediated apoptosis and anti-inflammatory pathway against diethylnitrosamine (DEN) induced HCC.Materials and methodsChemical carcinogenesis in Wistar rats was introduced by an intra-peritoneal dose of DEN (200 mg/kg). The rats received the various doses of GLA for 22 weeks. The progressions of serum biomarkers and histopathology components of hepatic tissue were used to access the prophylactic effects. The antioxidant parameters, cancer preventive agent status, and apoptosis mechanism were reviewed to scrutinize the possible mechanism.ResultsDose-dependent treatment of GLA significantly (P<−0.001) modulated the hepatic nodules, hepatic, body weight, antioxidant, and non-hepatic parameters. Curiously, the Real-time polymerase chain reaction (RT-PCR) and immunoblotting showed the GLA altered reduced the hypoxic microenvironment, mitochondrial mediated death apoptosis, and anti-inflammsatory pathways.ConclusionOn the basis of the above results, we can conclude that the GLA exhibited a chemo-protective effect against DEN induced HCC that might be due to the altered hypoxic microenvironment, mitochondrial mediated death apoptosis, and anti-inflammatory pathway, respectively.

show abstract

Section: Introductionmentioning

confidence: 91%

Gamma linolic acid regulates PHD2 mediated hypoxia and mitochondrial apoptosis in DEN induced Hepatocellular carcinoma

Cui

Han

Zhang

et al. 2018

DDDT

View full text Add to dashboard Cite

show abstract

“…Lipids, particularly polyunsaturated fatty acids, are susceptible to oxidation by oxygen free radicals, leading to lipid peroxidation that is harmful to cells and tissues [ 251 – 253 ]. Lipid peroxides are associated with many pathological states, including inflammation, neurodegenerative disease, cancer, and ocular and kidney degeneration [ 253 , 254 ].…”

Section: Introductionmentioning

confidence: 99%

Lipid metabolism reprogramming and its potential targets in cancer

Cheng

Geng

Cheng

et al. 2018

Cancer Communications

533

462

View full text Add to dashboard Cite

Reprogramming of lipid metabolism is a newly recognized hallmark of malignancy. Increased lipid uptake, storage and lipogenesis occur in a variety of cancers and contribute to rapid tumor growth. Lipids constitute the basic structure of membranes and also function as signaling molecules and energy sources. Sterol regulatory element-binding proteins (SREBPs), a family of membrane-bound transcription factors in the endoplasmic reticulum, play a central role in the regulation of lipid metabolism. Recent studies have revealed that SREBPs are highly up-regulated in various cancers and promote tumor growth. SREBP cleavage-activating protein is a key transporter in the trafficking and activation of SREBPs as well as a critical glucose sensor, thus linking glucose metabolism and de novo lipid synthesis. Targeting altered lipid metabolic pathways has become a promising anti-cancer strategy. This review summarizes recent progress in our understanding of lipid metabolism regulation in malignancy, and highlights potential molecular targets and their inhibitors for cancer treatment.

show abstract

“…9 Among the various key factors, tissues GSH depletion and cellular damaging effects of OFR are the key factors that lead to lipid peroxidation. 10,11 Therefore, in the pathogenesis of kidney damage, increased level of apoptosis may underline the main cause. Moreover, oxidative stress and inflammation are closely linked to each other and are distinctive features of kidney problems.…”

Section: Introductionmentioning

confidence: 99%

Roflumilast, a phosphodiesterase 4 inhibitor, attenuates cadmium-induced renal toxicity via modulation of NF-κB activation and induction of NQO1 in rats

et al. 2019

View full text Add to dashboard Cite

Objective: In the present study, the protective effect of Roflumilast (ROF, a selective phosphodiesterase (PDE-4) inhibitor) was investigated against cadmium (Cd)-induced nephrotoxicity in rats. Methods: A total of 24 rats were selected and randomly divided into four groups ( n = 6). Group 1 served as the control; groups 2–4 administered with CdCl2 (3 mg/kg, i.p.) for 7 days; groups 3 and 4 were co-administered with ROF in doses of 0.5 and 1.5 mg/kg, orally for 7 consecutive days. Nephrotoxicity was evaluated by measuring urine volume, urea and creatinine levels in urine and serum. Oxidative stress was confirmed by measuring malondialdehyde (MDA), glutathione (GSH), superoxide dismutase (SOD), and catalase (CAT) levels in kidney tissue followed by histopathological studies. Results: CdCl2 administration results in a significant ( p < 0.01) decrease in urine volume, urea, and creatinine levels in urine, as well as GSH, SOD, and CAT levels in renal tissue. In addition, Cd also produced significantly increased ( p < 0.01) urea and creatinine levels in serum and TBARS levels in renal tissues. Rats treated with ROF significantly ( p < 0.01) restore the altered levels of kidney injury markers, nonenzymatic antioxidant, as well as depleted enzymes in dose-dependent manner. An increased expression of NF-κB p65 and decreased expression of GST and NQO1 in the Cd only treated group were significantly reversed by high dose of ROF (1.5 mg/kg). Histopathological changes were also ameliorated by ROF administration in Cd-treated groups. Conclusion: In conclusion, ROF treatment showed protective effect against renal damage and increased oxidative stress induced by Cd administration.

show abstract

Modulation of oxidative stress response by flaxseed oil: Role of lipid peroxidation and underlying mechanisms

Cited by 54 publications

References 56 publications

Gamma linolic acid regulates PHD2 mediated hypoxia and mitochondrial apoptosis in DEN induced Hepatocellular carcinoma

Gamma linolic acid regulates PHD2 mediated hypoxia and mitochondrial apoptosis in DEN induced Hepatocellular carcinoma

Lipid metabolism reprogramming and its potential targets in cancer

Roflumilast, a phosphodiesterase 4 inhibitor, attenuates cadmium-induced renal toxicity via modulation of NF-κB activation and induction of NQO1 in rats

Contact Info

Product

Resources

About