Scholarlink

<p>Caffeic acid (CA) is known to inhibit LPS-induced NF-κB activation in endothelial cells, potentially down regulating matrix metalloproteinases (MMPs), and limiting oxidative and inflammatory responses. Despite this, direct evidence supporting the involvement of LPS→NF-κB→MMP-1/13 pathway as a target of CA is limited. Meanwhile its effects on gastrointestinal inflammation, thyroid and liver homeostasis, and interplay between intestinal alkaline phosphatase (ALP) activity and iodine absorption during such inflammatory/toxic conditions also remains to be established. For this study, female swiss albino mice (25–27 gram) were allocated into six treatment-groups (6 animal/group): (Group I) control; received isotonic-saline (0.9% NaCl) throughout the experimental duration, (Group II, III, IV): exposed with LPS (1&#xa0;mg/kg BW, for 5 days). From day-6, group III, V received CA low dose (10&#xa0;mg/kg BW); group IV, VI received CA high dose (20&#xa0;mg/kg BW) for another 28-days. Both the LPS and CA were administered intraperitoneally (i.p.) Outcomes included status of oxidative stress, plasma expression of NF-κB, IL-10, TNF-α, ALP, AST, ALT, serum iodine level, thyroid hormone status, and histopathology. Molecular docking of CA with catalytic residues of MMP-1/13 was performed to assess binding affinity and interaction features. CA, dose-dependently suppressed LPS-induced NF-κB and pro-inflammatory cytokines activation, restored ALP activity &amp; iodine absorption, ameliorated liver enzyme, thyroid hormone disruption, and improved histology. In silico verdict suggests mechanistic observation where CA may directly inhibit MMP-1/13 via binding to their catalytic residues. These findings suggest CA’s potential as a phytotherapeutic agent via mitigating the LPS→NF-κB→MMP-1/13 cascade and preservation of gut-thyroid-liver homeostasis under inflammatory/toxic condition.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Breaking the Inflammatory Loop: Caffeic Acid Inhibits LPS/NF-κB/MMPs pathway and Preserves ALP-Iodine Crosstalk in LPS Induced Murine Endocrinopathy

  • 期刊论文

  • 发表日期：

    2026年4月11日

查看全文
  • Anjali Yadav,
  • Banalata Mohanty

摘要

Caffeic acid (CA) is known to inhibit LPS-induced NF-κB activation in endothelial cells, potentially down regulating matrix metalloproteinases (MMPs), and limiting oxidative and inflammatory responses. Despite this, direct evidence supporting the involvement of LPS→NF-κB→MMP-1/13 pathway as a target of CA is limited. Meanwhile its effects on gastrointestinal inflammation, thyroid and liver homeostasis, and interplay between intestinal alkaline phosphatase (ALP) activity and iodine absorption during such inflammatory/toxic conditions also remains to be established. For this study, female swiss albino mice (25–27 gram) were allocated into six treatment-groups (6 animal/group): (Group I) control; received isotonic-saline (0.9% NaCl) throughout the experimental duration, (Group II, III, IV): exposed with LPS (1 mg/kg BW, for 5 days). From day-6, group III, V received CA low dose (10 mg/kg BW); group IV, VI received CA high dose (20 mg/kg BW) for another 28-days. Both the LPS and CA were administered intraperitoneally (i.p.) Outcomes included status of oxidative stress, plasma expression of NF-κB, IL-10, TNF-α, ALP, AST, ALT, serum iodine level, thyroid hormone status, and histopathology. Molecular docking of CA with catalytic residues of MMP-1/13 was performed to assess binding affinity and interaction features. CA, dose-dependently suppressed LPS-induced NF-κB and pro-inflammatory cytokines activation, restored ALP activity & iodine absorption, ameliorated liver enzyme, thyroid hormone disruption, and improved histology. In silico verdict suggests mechanistic observation where CA may directly inhibit MMP-1/13 via binding to their catalytic residues. These findings suggest CA’s potential as a phytotherapeutic agent via mitigating the LPS→NF-κB→MMP-1/13 cascade and preservation of gut-thyroid-liver homeostasis under inflammatory/toxic condition.