Lab Anim Res.  2022 Dec;38(4):329-336. 10.1186/s42826-022-00148-x.

Chlorogenic acid attenuates pro‑inflammatory response in the blood of streptozotocin‑induced diabetic rats

• Lee Y
• Bae C
• Ahn T

• KMID: 2537636
• DOI: http://doi.org/10.1186/s42826-022-00148-x

Abstract

Background
Chlorogenic acid (CGA) has been shown to reduce pro-inflammation by scavenging reactive oxy‑ gen species (ROS) and reactive nitrogen species. In this study, the anti-inflammatory effect of CGA was expanded to streptozotocin (STZ)-induced diabetic rats. The inter-relationships among oxidative stress, pro-inflammation, and cytochrome P450 (CYP) 1A enzymes were also investigated in peripheral blood mononuclear cells (PBMC) of STZdiabetic rats.
Results
The levels of pro-inflammatory cytokines, interleukin-6 and tumor necrosis factor-alpha, increased by approximately 3.4- and 2.9-fold, respectively, and the albumin concentration decreased in the serum of STZ-induced diabetic rats compared to normal rats. The C-reactive protein (CRP) values also increased by about 3.8-fold higher, indicating that STZ induced an inflammation in the blood of STZ-diabetic rats. The expression levels and catalytic activities of CYP1A enzymes were elevated by approximately 2.2–2.5- and 4.3–6.7-fold, respectively, in the PBMC of STZ-treated rats. A decrease in the amount of PBMC-bound albumin was also observed. In contrast, the levels of cytokines and CRP in serum and the activities of CYP1A enzymes in PBMC were significantly reduced in CGA-treated diabetic rats in a CGA concentration-dependent manner. In addition, STZ-mediated elevation of ROS in serum and PBMC was decreased by the CGA administration. However, the CGA treatment did not change the enhanced blood glucose level and expression of CYP1A enzymes by STZ. STZ-mediated decrease in the levels of serum and PBMCbound albumin was not also restored by the CGA administration.
Conclusions
These results suggest that CGA could be used to treat type 1 diabetes-induced inflammation.

Keyword

Chlorogenic acid; Cytochrome P450; Oxidative stress; Pro-inflammation