Epidermal Growth Factor, through Alleviating Oxidative Stress, Protect IPEC-J2 Cells from Lipopolysaccharides-Induced Apoptosis

Tang, Xiangwei; Liu, Bo; Wang, Xiangrong; Yu, Qifang; Fang, Rejun

doi:10.3390/ijms19030848

Cited by 72 publications

(66 citation statements)

References 52 publications

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“…Various studies indicate the antitumor effects of H. pluvialis extract, which is rich in astaxanthin, being a potent growth inhibitor under laboratory conditions [16]. The results of the present study show anti-proliferative effects of astaxanthin seen by the increase in the expression of caspase 3, Bax, antioxidant activity conversely, decreasing the expression of bcl2, and the level of malondialdehyde in the LS-180 cell line [17,18]. A study reported that daily administration of astaxanthin could be effective in preventing colon cancer [19].…”

Section: Discussionsupporting

confidence: 63%

Astaxanthin induces apoptosis and increases activity of antioxidant enzymes in LS-180 cells

Hadipour

Ghoreishi

Baharvand

2019

Artificial Cells, Nanomedicine, and Biotechnology

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Astaxanthin, a Xanthophyll carotenoid, has strong antioxidant properties. Some studies have shown the effectiveness of this compound on the prevention and treatment of cancer. Therefore, the aim of this study was to evaluate the effects of astaxanthin on induction of apoptosis and antioxidant activity in the LS-180 cell line. In this experimental study, after the treatment of LS-180 50, 100 and 150 lm of Astaxanthin for 24 h, the expression levels of Bax, Bcl2 and Caspase3 genes were investigated by Realtime PCR. Also, the level of malondialdehyde, as an indicator of oxidative stress and activity of antisuperoxide dismutase enzymes, catalase and glutathione peroxidase was investigated by colorimetric methods. The results showed that astaxanthin increases the expression of Bax and Caspase3 genes and decreases that of Bcl2, thereby, inducing apoptosis and inhibiting growth and proliferation of the cells. Additionally, reduction in the levels of malondialdehyde was evident with a significant elevation in antioxidant activity mediated by the action of superoxide dismutase, catalase and glutathione peroxidase. These results suggest that astaxanthin has the potency to induce apoptosis in LS-180 cells by increasing the expression of apoptotic genes and activity of antioxidant enzymes. Thus, astaxanthin has potential in the prevention and treatment of cancer. ARTICLE HISTORY

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Section: Discussionsupporting

confidence: 63%

Astaxanthin induces apoptosis and increases activity of antioxidant enzymes in LS-180 cells

Hadipour

Ghoreishi

Baharvand

2019

Artificial Cells, Nanomedicine, and Biotechnology

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“…In previous studies, controversies still existed on whether LPS affect the viability and morphology of various cells. Different from Tang's results [12], in present study, the relative activity and morphology of cells exposed to 1, 5, and 10 µg/mL of LPS was not remarkably changed in comparison with the control group. However, Lee's results were similar to that of this research, where after continuous treatment with 1 µg/mL LPS for 24 h, the viability of HT29 and RAW264.7 cells showed no obvious changes, despite the different cell lines used [13].…”

Section: Discussioncontrasting

confidence: 99%

Quercetin inhibits porcine intestinal inflammation <i>in vitro</i>

Chen¹,

Xu²,

Yuan³

et al. 2019

Trop. J. Pharm Res

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Purpose: To investigate the effect of Quercetin (Que) on inflammatory reaction in intestinal porcine enterocyte cells, IPEC-J2, induced by lipopolysaccharide (LPS). Methods: IPEC-J2 cells were pretreated with Que and then incubated with LPS. Cell viability, cell morphology, nitric oxide (NO) content, gene expression levels of interleukin-6 (IL-6) and interleukin-8 (IL-8), were then evaluated. Results: LPS incubation at 10 μg/mL for 24 h showed no effect on the viability and cell morphology of IPEC-J2, while Que pre-incubation significantly enhanced the viability of IPEC-J2 and improved cell morphology (p < 0.05). Que decreased the expression levels of pro-inflammatory cytokines IL-6 mRNA and IL-8 mRNA raised by LPS (p < 0.05). Interestingly, both LPS and Que demonstrated no influence on the release of NO. Conclusion: Pre-treatment of Que shows a positive effect on intestinal porcine enterocyte cells and inhibited porcine intestinal inflammation in vitro induced by LPS, but the mechanism may be not associated with NO-related signaling pathway. Therefore, Que might have a potential effect as a veterinary drug or feed additive for the treatment of enteritis in pigs.

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“…Once cells are exposed to oxidative stress, Nrf2 translocates into the nucleus and activates the transcription of genes containing ARE, such as heme oxygenase-1 (HO-1), glutathione S-transferase (GST) and thioredoxin reductase (TrxR). After being activated, the ARE-containing genes play their biologic role in antioxidant (Li et al, 2018b;Gan and Johnson, 2014;Tang et al, 2018). The significant effects of Nrf2 against oxidative stress-induced diseases have been verified.…”

Section: Discussionmentioning

confidence: 96%

Procyanidin protects HK-2 cells against cisplatin-induced injury through antioxidant action involving Nrf2/HO-1 signaling pathway

Chen

Feng

Jing

et al. 2019

Fundam. Toxicol. Sci.

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-Cisplatin (CP) is used as a chemotherapeutic drug for the treatment of various kinds of cancer. However, it is becoming increasingly difficult to ignore its side effects, especially nephrotoxicity which has to do with oxidative stress and inflammation. Procyanidin (PRO) has been proved to be a powerful antioxidant. Therefore, we investigated whether PRO could prevent Cisplatin-induced nephrotoxicity and explored the underlying mechanism. In cellular experiment, reactive oxygen species (ROS), the malondialdehyde (MDA) levels, the activities of total superoxide dismutase (T-SOD) and glutathione peroxidase (GSH-PX) were measured for the assessment of cisplatin-induced oxidative cell damage. CCK-8 reagent and flow cytometry were used to detect the cell viability and apoptosis. Furthermore, the level of oxidative-related protein Nrf2 and HO-1 were carried out by western blot analysis. We found that cisplatin gave rise to the elevated levels of ROS and MDA and the decrease of the activities of T-SOD and GSH-PX with a related lower viability and higher apoptosis in HK-2 cells. Inversely, the pretreatment of PRO mitigated the oxidative damage, promoted the cell viability and lowered the apoptosis, activated nuclear related factor 2 (Nrf2) and elevated the expression of heme oxygenase-1 (HO-1), the above cytoprotection of PRO was blocked by siNrf2 or siHO-1. These results demonstrated that PRO has the potential to prevent cisplatin-induced nephrotoxicity through activation of Nrf2/HO-1 signaling pathway.

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Epidermal Growth Factor, through Alleviating Oxidative Stress, Protect IPEC-J2 Cells from Lipopolysaccharides-Induced Apoptosis

Cited by 72 publications

References 52 publications

Astaxanthin induces apoptosis and increases activity of antioxidant enzymes in LS-180 cells

Astaxanthin induces apoptosis and increases activity of antioxidant enzymes in LS-180 cells

Quercetin inhibits porcine intestinal inflammation <i>in vitro</i>

Procyanidin protects HK-2 cells against cisplatin-induced injury through antioxidant action involving Nrf2/HO-1 signaling pathway

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