Effect of chlorogenic acid on alleviating inflammation and apoptosis of IPEC-J2 cells induced by deoxyniyalenol

Xu, Xiaoxiang; Chang, Juan; Wang, Ping; Yin, Qingqiang; Liu, Chaoqi; Li, Maolong; Song, Andong; Zhu, Qun; Lu, Fushan

doi:10.1016/j.ecoenv.2020.111376

Cited by 35 publications

(31 citation statements)

References 49 publications

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“…Consistent with these studies, CGA increased the antioxidant ability and reduced the expression of proinflammatory cytokines of duodenum in our study indicated by the increased activities of T‐AOC and T‐SOD and the decreased expression of IL‐1β and TNFα . Although Xu et al (2020) reported that CGA could increase the mRNA abundance and protein expression of ZO‐1 and CLDN1 of IPEC‐J2 cells treated by deoxynivalenol (Xu et al, 2020), no similar results were found in this study.…”

Section: Discussioncontrasting

confidence: 77%

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Effect of chlorogenic acid on intestinal inflammation, antioxidant status, and microbial community of young hens challenged with acute heat stress

Zhang

Zhao

Yang

et al. 2021

Animal Science Journal

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Heat stress in poultry is deleterious to productive performance. Chlorogenic acid (CGA) exerts antibacterial, anti-inflammatory, and antioxidant properties. This study was conducted to evaluate the effects of dietary supplemental CGA on the intestinal health and cecal microbiota composition of young hens challenged with acute heat stress. 100-day-old Hy-line brown pullets were randomly divided into four groups.The control group (C) and heat stress group (HS) received a basal diet. HS + CGA 300 group and HS + CGA 600 group received a basal diet supplemented with 300-and 600-mg/kg CGA, respectively, for 2 weeks before heat stress exposure. Pullets of HS, HS + CGA 300 , and HS + CGA 600 group were exposed to 38 C for 4 h while the control group was maintained at 25 C. In this study, dietary CGA supplementation had effect on mitigate the decreased T-AOC and T-SOD activities and the increasing of IL-1β and TNFα induced by acute heat stress. Dietary supplementation with 600 mg/kg CGA had better effect on increasing the relative abundance of beneficial bacterial genera, such as Rikenellaceae RC9_gut_group, Ruminococcaceae UCG-005, and Christensenellaceae R-7_group, and deceasing bacteria genera involved in inflammation, such as Sutterella species. Therefore, CGA can ameliorate acute heat stress damage through suppressing inflammation and improved antioxidant capacity and cecal microbiota composition.

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Section: Discussioncontrasting

confidence: 77%

“…Although Xu et al (2020) reported that CGA could increase the mRNA abundance and protein expression of ZO-1 and CLDN1 of IPEC-J2 cells treated by deoxynivalenol (Xu et al, 2020), no similar results…”

Section: Effects Of Acute Heat Stress and Chlorogenic Acid Supplementation On Cecal Microbiota Communitymentioning

confidence: 96%

Effect of chlorogenic acid on intestinal inflammation, antioxidant status, and microbial community of young hens challenged with acute heat stress

Zhang

Zhao

Yang

et al. 2021

Animal Science Journal

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“…LDH is an important indicator of the intestinal epithelial barrier integrity. It is known that LDH is released when the cells are damaged, so LDH release can indirectly reflect the permeability of cells (33). In the present study, TGEV infection significantly increased the LDH activity in IPEC-J2 cells culture medium, whereas ATRA treatment significantly decreased LDH released from the TGEVinfected IPEC-J2 cells.…”

Section: Discussionsupporting

confidence: 43%

All-Trans Retinoic Acid Attenuates Transmissible Gastroenteritis Virus-Induced Inflammation in IPEC-J2 Cells via Suppressing the RLRs/NF‐κB Signaling Pathway

Chen

Tian

et al. 2022

Front. Immunol.

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Transmissible gastroenteritis virus (TGEV) infection can cause transmissible gastroenteritis (TGE), especially in suckling piglets, resulting in a significant economic loss for the global pig industry. The pathogenesis of TGEV infection is closely related to intestinal inflammation. All-trans retinoic acid (ATRA) has anti-inflammatory activity and immunomodulatory properties, but it is unclear whether ATRA can attenuate the inflammatory response induced by TGEV. This study aimed to investigate the protective effect of ATRA on TGEV-induced inflammatory injury in intestinal porcine epithelial cells (IPEC-J2) and to explore the underlying molecular mechanism. The results showed that TGEV infection triggered inflammatory response and damaged epithelial barrier integrity in IPEC-J2 cells. However, ATRA attenuated TGEV-induced inflammatory response by inhibiting the release of pro-inflammatory cytokines, including IL-1β, IL-6, IL-8 and TNF-α. ATRA also significantly reversed the reduction of ZO-1 and Occludin protein levels induced by TGEV infection and maintained epithelial barrier integrity. Moreover, ATRA treatment significantly prevented the upregulation of IкBα and NF-κB p65 phosphorylation levels and the nuclear translocation of NF-кB p65 induced by TGEV. On the other hand, treatment of TGEV-infected IPEC-J2 cells with the NF-κB inhibitors (BAY11-7082) significantly decreased the levels of inflammatory cytokines. Furthermore, ATRA treatment significantly downregulated the mRNA abundance and protein levels of TLR3, TLR7, RIG-I and MDA5, and downregulated their downstream signaling molecules TRIF, TRAF6 and MAVS mRNA expressions in TGEV-infected IPEC-J2 cells. However, the knockdown of RIG-I and MDA5 but not TLR3 and TLR7 significantly reduced the NF-κB p65 phosphorylation level and inflammatory cytokines levels in TGEV-infected IPEC-J2 cells. Our results indicated that ATRA attenuated TGEV-induced IPEC-J2 cells damage via suppressing inflammatory response, the mechanism of which is associated with the inhibition of TGEV-mediated activation of the RLRs/NF‐κB signaling pathway.

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“…CGA significantly inhibited COX-2 expression under ammonia stress in the present study. A large sample of previous studies confirmed that CGA could markedly suppress the expression of COX-2 in deoxyniyalenolinduced IPEC-J2 cells (Xu et al, 2020), methotrexate-induced rat liver (Nemat et al, 2017), cisplatin-induced mice kidney (Domitrović et al, 2014), and LPS-induced RAW 264.7 cells (Hwang et al, 2014).…”

Section: Discussionmentioning

confidence: 83%

“…CGA significantly inhibited COX‐2 expression under ammonia stress in the present study. A large sample of previous studies confirmed that CGA could markedly suppress the expression of COX‐2 in deoxyniyalenol‐induced IPEC‐J2 cells (Xu et al, 2020), methotrexate‐induced rat liver (Nemat et al, 2017), cisplatin‐induced mice kidney (Domitrović et al, 2014), and LPS‐induced RAW 264.7 cells (Hwang et al, 2014). This indicated that ammonia could further activate inflammation by activating NF‐κB / COX‐2 signaling pathway, and CGA suppressed inflammatory response by inhibiting NF‐κB / COX‐2 signaling pathway.…”

Section: Discussionmentioning

confidence: 84%

Chlorogenic acid attenuates inflammation, oxidative stress, apoptosis and protects head kidney macrophage of yellow catfish from ammonia toxicity

Jiang

Luo

et al. 2021

Aquaculture Research

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Ammonia is the most common contaminants found in aquaculture water that seriously endangers fish health. However, there are few studies on the strategy and mechanism on alleviating ammonia toxicity in fish. The current study aimed to observe the cytotoxic effects of ammonia and the protective effects of chlorogenic acid (CGA) on head kidney macrophage of yellow catfish from the perspective of inflammation, oxidative stress and apoptosis. The cells were randomized into normal control, ammonia group (0.23 mg L −1 ), CGA group (125 µmol L −1 ), CGA (5, 25, 125 µmol L −1 ) + ammonia (0.23 mg L −1 ) groups. Cells were pretreated with CGA for 1 h followed by ammonia for 24 h. Findings suggested that ammonia treatment reduced cell viability, increased ROS production, up-regulated antioxidant (SOD, GPx) and pro-inflammatory (TNFα, IL-1, IL-6, COX-2, NF-κB p65) genes expression, down-regulated the mRNA levels of M2-type macrophage marker (Arg-1) and anti-apoptosis (Bcl-2), and CGA attenuated the toxic effects of ammonia. The findings may provide insight into the underlying mechanisms of ammonia toxicity and suggest that CGA can be used as a potential natural supplement to alleviate ammonia toxicity in fish.

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Effect of chlorogenic acid on alleviating inflammation and apoptosis of IPEC-J2 cells induced by deoxyniyalenol

Cited by 35 publications

References 49 publications

Effect of chlorogenic acid on intestinal inflammation, antioxidant status, and microbial community of young hens challenged with acute heat stress

Effect of chlorogenic acid on intestinal inflammation, antioxidant status, and microbial community of young hens challenged with acute heat stress

All-Trans Retinoic Acid Attenuates Transmissible Gastroenteritis Virus-Induced Inflammation in IPEC-J2 Cells via Suppressing the RLRs/NF‐κB Signaling Pathway

Chlorogenic acid attenuates inflammation, oxidative stress, apoptosis and protects head kidney macrophage of yellow catfish from ammonia toxicity

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