Pharmacologic overview of systemic chlorogenic acid therapy on experimental wound healing

Abstract

Chlorogenic acid (CGA) is a well-known natural antioxidant in human diet. To understand the effects of CGA on wound healing by enhancing antioxidant defense in the body, the present study sought to investigate the potential role of systemic CGA therapy on wound healing and oxidative stress markers of the skin. We also aimed to understand whether chronic CGA treatment has side effects on pivotal organs or rat bone marrow during therapy. Full-thickness experimental wounds were created on the backs of rats. CGA (25, 50, 100, 200 mg/kg) or vehicle was administered intraperitoneally for 15 days. All rats were sacrificed on the 16th day. Biochemical, histopathological, and immunohistochemical examinations were performed. Possible side effects were also investigated. The results suggested that CGA accelerated wound healing in a dose-dependent manner. CGA enhanced hydroxyproline content, decreased malondialdehyde and nitric oxide levels. and elevated reduced glutathione, superoxide dismutase, and catalase levels in wound tissues. Epithelialization, angiogenesis, fibroblast proliferation, and collagen formation increased by CGA while polymorph nuclear leukocytes infiltration decreased. CGA modulated matrix metalloproteinase-9 and tissue inhibitor-2 expression in biopsies. Otherwise, high dose of CGA increased lipid peroxidation of liver and kidney without affecting the heart and muscle samples. Chronic CGA increased micronuclei formation and induced cytotoxicity in the bone marrow. In conclusion, systemic CGA has beneficial effects in improving wound repair. Antioxidant, free radical scavenger, angiogenesis, and anti-inflammatory effects of CGA may ameliorate wound healing. High dose of CGA may induce side effects. In light of these observations, CGA supplementation or dietary CGA may have benefit on wound healing.

Caffeic acid and chlorogenic acid: Evaluation of antioxidant effect and inhibition of key enzymes linked with hypertension

“…The peroxynitrite is capable of initiating lipid peroxidation, inflammation, cancer, and other pathological condition (Bates, Baker, Guerra, & Harrison, ). The observed results from this finding also agree with other studies on the inhibitory effects of caffeic acid and chlorogenic acid on MDA level and their anti‐inflammatory effects during wound healing in experimental animals (Bagdas et al, ; Gul, Demircan, Bagdas, & Buyukuysal, ). Furthermore, as revealed in Figure , caffeic and chlorogenic acid also exhibit NO radical scavenging ability, which can prevent peroxynitrite formation, reduce the potential for lipid peroxidation in the heart, and protect the heart membrane integrity.…”

An investigation on the in vitro wound healing activity and phytochemical composition of Hypericum pseudolaeve Robson growing in Turkey

“…Chlorogenic acid and quercitrin were also shown to have wound healing potential. 50,51 Our results and the data in the literature show that phenolic compounds may have important role in the wound healing potential of Hypericum genus. Study limitations Crude methanolic and aqueous extracts of H. pseudolaeve were investigated for their in vitro wound healing activity, antioxidant activity and phytochemical content.…”

Consumption of Chlorogenic Acids through Coffee and Health Implications

“…The reduction of inflammation resulting in enhanced wound healing has also been reported for CGA in different studies [111]. In a study with diabetic rats, the oral administration of 5-CQA enhanced hydroxyproline and decreased malondialdehyde/nitric oxide levels in wound tissues, in addition to elevating reduced-glutathione [143,144]. Another in vivo study using a mice skin excision wound showed that topically administrated hydrogels containing 5-CQA reduced significantly the wound area size in the inflammatory phase, enhancing the wound healing process [145].…”

“…In both cases, suppression of pro-inflammatory cytokines was observed. CGA (5-CQA) could effectively prevent mice from concanavalin A-induced hepatitis, which might have resulted from the activation of Toll-Like Receptor (TLR) 4 signaling, downregulating the expression of adhesion molecules, and also alleviating the infiltration and activation of hepatic leukocytes and the production of pro-inflammatory cytokines [143].…”