RETRACTED ARTICLE: Glycyrrhizic acid ameliorates submandibular gland oxidative stress, autophagy and vascular dysfunction in rat model of type 1 diabetes

Abstract

The burden of diabetes mellitus (DM) and associated complications is increasing worldwide, affecting many organ functionalities including submandibular glands (SMG). The present study aims to investigate the potential ameliorative effect of glycyrrhizic acid (GA) on diabetes-induced SMG damage. Experimental evaluation of GA treatment was conducted on a rat model of type I diabetes. Animals were assigned to three groups; control, diabetic and GA treated diabetic groups. After 8 weeks, the SMG was processed for assessment of oxidative stress markers, autophagy related proteins; LC3, Beclin-1 and P62, vascular regulator ET-1, aquaporins (AQPs 1.4 and 5), SIRT1 protein expressions in addition to LC3 and AQP5 mRNA expressions. Also, parenchymal structures of the SMG were examined. GA alleviated the diabetes-induced SMG damage via restoring the SMG levels of oxidative stress markers and ET-1 almost near to the normal levels most probably via regulation of SIRT1, AQPs and accordingly LC-3, P62 and Beclin-1levels. GA could be a promising candidate for the treatment of diabetes-induced SMG damage via regulating oxidative stress, autophagy and angiogenesis.

Role of Dapagliflozin and Liraglutide on Diabetes-Induced Cardiomyopathy in Rats: Implication of Oxidative Stress, Inflammation, and Apoptosis

“…Diabetes mellitus (DM) is a complex chronic metabolic disease whose incidence is escalating globally (1,2). Type 1 DM (T1DM) is caused by progressive T cell-mediated immune damage of pancreatic b cells resulting in persistent hyperglycemia (3).…”

Glycyrrhizin regulates antioxidation through Nrf2 signaling pathway in rat temporomandibular joint osteoarthritis

“…Consistent with the results of this study, SOD and CAT activities were significantly reduced in the neurodegenerative disease model, accompanied by elevated levels of the lipid peroxidation product and increased expression of COX2 and iNOS, whereas GL increased antioxidant enzyme activity, inhibited lipid peroxidation, and attenuated elevated levels of COX2 and iNOS, these results suggest that the neuroprotective effects of GL are attributed to its potent antioxidant and anti‐inflammatory properties 25 . Another study showed that diabetes caused an increase in malondialdehyde levels and a decrease in SOD and glutathione in submandibular gland tissue, however, GL reduced oxidative stress damage in submandibular gland tissue by restoring the levels of oxidative stress markers 26 …”

“…25 Another study showed that diabetes caused an increase in malondialdehyde levels and a decrease in SOD and glutathione in submandibular gland tissue, however, GL reduced oxidative stress damage in submandibular gland tissue by restoring the levels of oxidative stress markers. 26 The balance between oxidation and antioxidation is essential for maintaining healthy cartilage tissue, and disruption of this balance leads to OA pathogenesis and progression, with multiple enzymes and factors involved in the antioxidant process. In joint tissues, excessive oxidative stress not only causes abnormal bone and cartilage metabolism, leading to destruction of joint structures, but also stimulates cells in synovium, such as synovial cells and nerve cells, which are the main cause of pain and muscle symptoms during OA progression.…”

Sepsis-induced AKI: From pathogenesis to therapeutic approaches

“…Glycyrrhizic acid (GA), a bioactive ingredient of licorice, has been demonstrated to exhibit immunoregulatory, antioxidant, anti-inflammatory, and antiviral properties in various diseases ( Li et al, 2021a ; Asseri et al, 2022 ; Qian et al, 2022 ). Zhao et al found GA inhibited the production of TNF-α, IL-1β, and IL-6, and suppressed oxidative stress and apoptosis through activation of the extracellular signal-regulated kinase (ERK)/NF-κB signaling pathway in LPS and CLP-induced septic rats ( Zhao et al, 2016a ; Zhao et al, 2016b ).…”