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Chlorogenic Acid Alleviates Chronic Stress-Induced Intestinal Damage by Inhibiting the P38MAPK/NF-κB Pathway
Journal of Agricultural and Food Chemistry ( IF 6.1 ) Pub Date : 2023-06-09 , DOI: 10.1021/acs.jafc.3c00953
Yuan Zhao 1 , Chaoran Wang 1 , Tianyuan Yang 1 , Guofeng Feng 1 , Haoyang Tan 1 , Xue Piao 1 , Dongni Chen 1 , Yu Zhang 1 , Wenjign Jiao 1 , Yongping Chen 1, 2 , Jichen Sha 1 , Honggang Fan 1
Affiliation  

Chronic stress can cause intestinal barrier damage. MAPK and NF-κB are closely related to it. Chlorogenic acid (CGA), a dietary polyphenol, has been shown to have intestinal protective effects, but whether by regulating MAPK and NF-κB is not known. Therefore, in this experiment, 24 Wistar rats were randomly divided into 4 groups (C group, CS group, CS + SB203580, and CS + CGA group). Rats in the CS group were restrained stress for 6 h per day for 21 days. Rats in the CS + SB203580 group were given SB203582 (0.5 mg/kg, intraperitoneal injection) 1 h before restraint stress every other day. Rats in the CS + CGA group were given CGA (100 mg/kg, gavage) 1 h before restraint stress. In chronic stress, intestinal barrier damage was evident, while being restored after CGA treatment. After chronic stress, the levels of p-P38 were increased (P < 0.01), while the levels of p-JNK and p-ERK were not changed. The levels of p-p38 were elevated after CGA treatment (P < 0.01). These results suggested that p38MAPK played an important role in chronic stress-induced intestinal injury, and CGA could inhibit p38MAPK activity. Therefore, we chose SB203582 (P38MAPK inhibitor) to elucidate the role of p38. After chronic stress, intestinal tight junction key proteins Occludin, ZO-1, and Claudin3 protein and gene expression were reduced (P < 0.01), while being elevated after CGA or SB203582 intervention (P < 0.05). After CGA treatment, the levels of p-IκB, p-p65, p-p38, and TNF-α were reduced (P < 0.01). SB203582 intervention reduced p-p65 and TNF-α levels significantly (P < 0.01). These results suggested that CGA could inhibit the NF-κB pathway by suppressing p38MAPK, thereby alleviating chronic stress-induced intestinal damage.

中文翻译:

绿原酸通过抑制 P38MAPK/NF-κB 通路减轻慢性压力引起的肠道损伤

慢性压力会导致肠道屏障受损。MAPK和NF-κB与其密切相关。绿原酸 (CGA) 是一种膳食多酚,已被证明具有肠道保护作用,但是否通过调节 MAPK 和 NF-κB 尚不清楚。因此,本实验将24只Wistar大鼠随机分为4组(C组、CS组、CS+SB203580、CS+CGA组)。CS组大鼠每天受到限制性应激6小时,持续21天。CS+SB203580组大鼠每隔一天在束缚应激前1 h给予SB203582(0.5 mg/kg,腹腔注射)。CS + CGA 组大鼠在约束应激前 1 h 给予 CGA(100 mg/kg,灌胃)。在慢性压力下,肠道屏障受损明显,但经过 CGA 治疗后可恢复。慢性应激后,p-P38 水平升高(P < 0.01),而 p-JNK 和 p-ERK 水平没有变化。CGA处理后p-p38水平升高(P <0.01)。这些结果表明p38MAPK在慢性应激诱导的肠道损伤中发挥重要作用,CGA可以抑制p38MAPK活性。因此,我们选择SB203582(P38MAPK抑制剂)来阐明p38的作用。慢性应激后,肠道紧密连接关键蛋白 Occludin、ZO-1 和 Claudin3 蛋白及基因表达量均降低(P < 0.01),而 CGA 或 SB203582 干预后则升高(P < 0.05)。CGA治疗后,p-IκB、p-p65、p-p38和TNF-α水平降低(P < 0.01)。SB203582 干预显着降低 p-p65 和 TNF-α 水平(P <0.01)。这些结果表明CGA可以通过抑制p38MAPK来抑制NF-κB通路,从而减轻慢性应激引起的肠道损伤。
更新日期:2023-06-09
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