Recent Publications

Recent Publications on Protocatechuic Acid

Protocatechuic Acid Research Related To The Prostate Gland

Protocatechuic acid ameliorates testosterone-induced benign prostatic hyperplasia through the regulation of inflammation and oxidative stress in castrated rats.

 2020 Mar 30:e22502. doi: 10.1002/jbt.22502.

https://www.ncbi.nlm.nih.gov/pubmed/32227675

Protocatechuic Acid Research Related To The Brain

Protocatechuic Acid Inhibits Vulnerable Atherosclerotic Lesion Progression in Older Apoe-/- Mice.

 2020 May 1;150(5):1167-1177. doi: 10.1093/jn/nxaa017
https://www.ncbi.nlm.nih.gov/pubmed/32047914

Kinga Krzysztoforska, Dagmara Mirowska-Guzel, Ewa Widy-Tyszkiewicz. Pharmacological effects of protocatechuic acid and its therapeutic potential in neurodegenerative diseases:

Review on the basis of in vitro and in vivo studies in rodents and humans. Nutritional Neuroscience 2019, 22 (2) , 72-82. DOI: 10.1080/1028415X.2017.1354543.

Biomed Pharmacother. 2018 Apr;100:147-155. doi: 10.1016/j.biopha.2018.01.107. Epub 2018 Feb 8.

Protocatechuic Acid Research Related To Blood Pressure

Antihypertensive and antioxidant effects of protocatechuic acid in deoxycorticosterone acetate-salt hypertensive rats.

Safaeian L1, Emami R2, Hajhashemi V2, Haghighatian Z3.

Author information

Abstract

Protocatechuic acid (PCA) is a natural antioxidant with beneficial cardiovascular properties. In this study, the effect of supplementation with PCA was investigated in deoxycorticosterone acetate (DOCA)-salt hypertension. Male Wistar rats received DOCA (25 mg/kg, s.c.) twice weekly and 1% NaCl in drinking water and simultaneously treated with PCA (50, 100 and 200 mg/kg, p.o.) for 4 weeks. Systolic blood pressure (SBP) was detected using tail-cuff method. Electrolytes including Na+, K+ and chloride, catalase activity, glutathione, total antioxidant capacity, malondialdehyde (MDA) and hydroperoxides concentration were measured in serum samples. Body and organs weight, water intake and, kidney and heart histopathology were also evaluated. Administration of PCA reversed the changes caused by DOCA-salt approximately at all doses. At the lowest dose, PCA significantly decreased SBP (132.5 ± 4.0 vs 152.3 ± 4.5 mmHg, P < .05), serum sodium (138.5  ± 1.52 vs 141 ± 1.50, P < .05) and chloride level (101.6 ± 1.47 vs 110 ± 1.39, P < .01) and raised serum potassium level (3.8 ± 0.09 vs 3.1 ± 0.17, P < .05) compared with DOCA-salt hypertensive rats. PCA increased serum catalase activity, total antioxidant capacity and glutathione concentration and reduced MDA and hydroperoxides levels. PCA also improved organ weight changes, reduced water intake and moderately prevented histopathological changes of kidney and heart upon DOCA-salt administration. The present study indicates the antihypertensive and antioxidant effects of PCA against DOCA-salt hypertension.

ScientificWorldJournal. 2014 Mar 16;2014:387640. doi: 10.1155/2014/387640. eCollection 2014.

Protocatechuic Acid Research Related To Liver

Modulating the p66shc signaling pathway with protocatechuic acid protects the intestine from ischemia-reperfusion injury and alleviates secondary liver damage.

Ma L1, Wang G1, Chen Z1, Li Z1, Yao J2, Zhao H1, Wang S1, Ma Z1, Chang H1, Tian X1.

Author information

Abstract
 

Intestinal ischemia-reperfusion (I/R) injury is a serious clinical pathophysiological process that may result in acute local intestine and remote liver injury. Protocatechuic acid (PCA), which has been widely studied as a polyphenolic compound, induces expression of antioxidative genes that combat oxidative stress and cell apoptosis. In this study, we investigated the effect of PCA pretreatment for protecting intestinal I/R-induced local intestine and remote liver injury in mice. Intestinal I/R was established by superior mesenteric artery occlusion for 45 min followed by reperfusion for 90 min. After the reperfusion period, PCA pretreatment markedly alleviated intestine and liver injury induced by intestinal I/R as indicated by histological alterations, decreases in serological damage parameters and nuclear factor-kappa B and phospho-foxo3a protein expression levels, and increases in glutathione, glutathione peroxidase, manganese superoxide dismutase protein expression, and Bcl-xL protein expression in the intestine and liver. These parameters were accompanied by PCA-induced adaptor protein p66shc suppression. These results suggest that PCA has a significant protective effect in the intestine and liver following injury induced by intestinal I/R. The protective effect of PCA may be attributed to the suppression of p66shc and the regulation of p66shc-related antioxidative and antiapoptotic factors.