Despite wide application of sodium nitrite (SN) as food additive, it exhibits considerable side effects on various body organs at high dose or chronic exposure. The aim of this study was to test whether Glycyrrhizic acid (GA) could ameliorate SN-induced toxicity in lung and submandibular salivary gland (SMG). A sample size of 30 adult male albino rats was randomly allocated into 3 groups. Group 1 served as control group. Rats were treated orally with 80 mg/kg of SN in group 2 or SN preceded by (15 mg/kg) GA in group 3. Lung & SMG tissues were used for oxidative stress assessment, examination of histopathological changes, fibrosis (MTC, TGF-β and α-SMA) and inflammation (TNF-α, IL-1β and CD-68). Concurrent administration of GA ameliorated pulmonary and salivary SN-induced toxicity via restoring the antioxidant defense mechanisms with reduction of MDA levels. GA reduced the key regulators of fibrosis TGF-β and α-SMA and collagen deposition. In addition to reduction of inflammatory cytokine (TNF-α, IL-1β) and macrophages recruitments, GA amended both pulmonary and salivary morphological changes. The present study proposed GA as a promising natural herb with antioxidant, anti-inflammatory and antifibrotic effects against pulmonary and salivary SN-induced toxicity.
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http://dx.doi.org/10.1177/0960327120964555 | DOI Listing |
Food Chem Toxicol
October 2024
Nourse Science Centre for Pet Nutrition, Wuhu, 241200, PR China. Electronic address:
Acta Pharmacol Sin
January 2024
Institute of Brain Science and Disease, School of Basic Medicine, Shandong Provincial Key Laboratory of Pathogenesis and Prevention of Neurological Disorders, Qingdao University, Qingdao, 266021, China.
Gut microbiota disturbance and systemic inflammation have been implicated in the degeneration of dopaminergic neurons in Parkinson's disease (PD). How the alteration of gut microbiota results in neuropathological events in PD remains elusive. In this study, we explored whether and how environmental insults caused early neuropathological events in the substantia nigra (SN) of a PD mouse model.
View Article and Find Full Text PDFCNS Neurosci Ther
October 2022
Key Laboratory of Basic Pharmacology of Ministry of Education and Joint International Research Laboratory of Ethnomedicine of Ministry of Education and Key Laboratory of Basic Pharmacology of Guizhou Province and Laboratory Animal Center, Zunyi Medical University, Zunyi, China.
Introduction: Current studies have documented neuroinflammation is implicated in Parkinson's disease. Recently, growing evidence indicated peripheral inflammation plays an important role in regulation of neuroinflammation and thus conferring protection against dopamine (DA) neuronal damage. However, the underlying mechanisms are not clearly illuminated.
View Article and Find Full Text PDFImmunopharmacol Immunotoxicol
June 2022
Department of Toxicology, School of Public Health, Harbin Medical University, Harbin, People's Republic of China.
Context: Parkinson's disease is a common chronic neurodegenerative disease characterized by massive loss of dopaminergic neurons in the substantia nigra. Neuroinflammation has been shown to play an important role in the pathogenesis of neurodegenerative diseases such as Parkinson's disease. The role of immune tolerance in neuroinflammation and neurodegenerative diseases induced by peripheral factors is unclear.
View Article and Find Full Text PDFInt J Mol Sci
January 2021
Department of Pathology, Case Western Reserve University, Cleveland, OH 44106, USA.
Mitochondrial dysfunction represents a critical event in the pathogenesis of Parkinson's disease (PD). Increasing evidence demonstrates that disturbed mitochondrial dynamics and quality control play an important role in mitochondrial dysfunction in PD. Our previous study demonstrated that MPP induces mitochondrial fragmentation in vitro.
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