Protocatechuic acid abrogates oxidative insults, inflammation, and apoptosis in liver and kidney associated with monosodium glutamate intoxication in rats

Abstract

Monosodium glutamate (MSG), a commonly used avor enhancer, has been reported to induce hepatic and renal dysfunctions. In this study, the palliative role of protocatechuic acid (PCA) in MSG-administered rats was elucidated. Adult male rats were assigned to four groups, namely control, MSG (4 mg/kg), PCA (100 mg/kg), and the last group was co-administered MSG and PCA at aforementioned doses for seven days. Results showed that MSG augmented the hepatic (AST and ALT) and renal (urea and creatinine) functions markers as well as glucose, triglycerides, total cholesterol and LDL levels. Moreover, marked increases in MDA levels accompanied by declines in GSH levels and notable decreases in the activities of SOD, CAT, GPx, and GR were observed in MSG-treated group. The MSG-mediated oxidative stress was further con rmed by down-regulation of Nfe2l2 gene expression levels in both tissues. In addition, MSG enhanced the hepatorenal in ammatory response as witnessed by increased in ammatory cytokines (IL-1b and TNF-α) and elevated NF-κB levels in both tissues. Further, signi cant increases in Bax (proapoptotic biomarker) levels together with decreases in Bcl-2 (anti-apoptotic marker) levels were observed in MSG administration. Hepatic and renal histopathological screening supported the biochemical and molecular ndings. On the contrary, co-treatment of rats with PCA resulted in remarkable enhancement of the antioxidant cellular capacity, suppression of in ammatory mediators and apoptosis. These effects are possibly endorsed for activation of Nrf-2 and suppression of NF-kB signaling pathways. Collectively, addition of PCA counteracted MSG-induced hepatic and renal injurious effects through modulation of oxidative, in ammatory and apoptotic alterations.

Protocatechuic acid and quercetin attenuate ETEC-caused IPEC-1 cell inflammation and injury associated with inhibition of necroptosis and pyroptosis signaling pathways

“…Although the beneficial effect of plant polyphenols on intestinal health has been studied, the research on PCA and Que regulating cell necrosis is very limited. Only reports from Chen et al who reported that Que inhibited TNF-α induced HUVECs apoptosis in human umbilical vein endothelial cells (HUVECs) after TNF-α stimulation [ 46 ] and Kassab et al who found PCA relived liver and kidney cell apoptosis in rats after monosodium glutamate intoxication [ 47 ]. These results indicate a novel and important role for plant polyphenols in inhibiting cell necrosis, which maybe ultimately contribute to improved barrier function.…”

Protocatechuic acid reverses myocardial infarction mediated by β‐adrenergic agonist via regulation of Nrf2/HO‐1 pathway, inflammatory, apoptotic, and fibrotic events

“…The antioxidative mode of action of PCA may refer to the activation of Nrf2 which control and regulate several genes involved in cellular antioxidant protection and detoxification. [ 12,21 ]…”

“…The antioxidative mode of action of PCA may refer to the activation of Nrf2 which control and regulate several genes involved in cellular antioxidant protection and detoxification. [12,21] Inflammation during and after MI has been recognized to have a critical role in its pathogenesis. According to earlier studies, ISO injection provoked substantial increases in TNF-α, IL-1β, and NF-κB in the cardiac tissue.…”

“…[2] Protocatechuic acid (PCA) is a polyphenolic metabolite distributed in fruits and vegetables such as Vitis vinifera, Olea europaea, and Oryza sativa and medicinal herbs including Salvia miltiorrhiza and Hibiscus sabdariffa. [12,13] Different experimental studies have highlighted PCA's various biological and pharmacological activities. [14,15] Oral administration of PCA significantly reduced systolic blood pressure and serum sodium and chloride in deoxycorticosterone acetate-salt-induced hypertension in a rat model.…”

Perspective: Might Maternal Dietary Monosodium Glutamate (MSG) Consumption Impact Pre- and Peri-Implantation Embryos and Their Subsequent Development?

“…Additionally, the culture of blastocysts in medium containing 5.0 mM glutamate, significantly reduces blastocyst cell numbers, especially in the ICM [ 7 ]. Since MSG intoxication causes apoptosis in rat liver and kidney [ 32 ], we suggest that excess glutamate also causes reduction in ICM cell number, in part, via apoptosis in the blastocyst ( Figure 1 ). The likely need for carefully regulated glutamate production and signaling in the blastocyst ICM are illustrated in Figure 1 .…”