Magnesium isoglycyrrhizinate alleviates liver injury in obese rats with acute necrotizing pancreatitis

Mei, Fangchao; Yu, Jie-Ping; Li, Man; Xiang, Mingwei; Hong, Yupu; Zhou, Yu; You, Yun-dong; Xia, He; Jin, Hongzhong; Wang, Weixing

doi:10.1016/j.prp.2018.10.030

Cited by 14 publications

(14 citation statements)

References 36 publications

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“…Following 3-day acclimation, rats were matched with basic body weight and allocated for 8 weeks under different diet treatments. After 8-week feeding on the SCD or HFD, the AP model was induced by a standardized retrograde infusion of 5% STC solution into the rat biliopancreatic duct as previously described [15]. General anesthetic to all rats was induced and maintained by inhaled isoflurane with oxygen during laparotomy.…”

Section: Methodsmentioning

confidence: 99%

High-Fat Diet Aggravates Acute Pancreatitis via TLR4-Mediated Necroptosis and Inflammation in Rats

Hong

et al. 2020

Oxidative Medicine and Cellular Longevity

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High-fat diet (HFD) often increases oxidative stress and enhances inflammatory status in the body. Toll-like receptor 4 (TLR4) is widely expressed in the pancreatic tissues and plays an important role in pancreatitis. This study is aimed at investigating the effect of HFD on acute pancreatitis (AP) and the role of TLR4-mediated necroptosis and inflammation in this disease. Weight-matched rats were allocated for an 8-week feeding on the standard chow diet (SCD) or HFD, and then, the AP model was induced by infusion of 5% sodium taurocholate into the biliopancreatic duct. Rats were sacrificed at an indicated time point after modeling. Additionally, inhibition of TLR4 signaling by TAK-242 in HFD rats with AP was conducted in vivo. The results showed that the levels of serum free fatty acid (FFA) in HFD rats were higher than those in SCD rats. Moreover, HFD rats were more vulnerable to AP injury than SCD rats, as indicated by more serious pathological damage and much higher pancreatic malondialdehyde (MDA) and lipid peroxidation (LPO) levels as well as lower pancreatic superoxide dismutase (SOD) activities and reduced glutathione (GSH) contents and more intense infiltration of MPO-positive neutrophils and CD68-positive macrophages. In addition, HFD markedly increased the expressions of TLR4 and necroptosis marker (RIP3) and aggravated the activation of NF-κB p65 and the expression of TNF-α in the pancreas of AP rats at indicated time points. However, TLR4 inhibition significantly attenuated the structural and functional damage of the pancreas induced by AP in HFD rats, as indicated by improvement of the above indexes. Taken together, these findings suggest that HFD exacerbated the extent and severity of AP via oxidative stress, inflammatory response, and necroptosis. Inhibition of TLR4 signaling by TAK-242 alleviated oxidative stress and decreased inflammatory reaction and necroptosis, exerting a protective effect during AP in HFD rats.

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Section: Methodsmentioning

confidence: 99%

High-Fat Diet Aggravates Acute Pancreatitis via TLR4-Mediated Necroptosis and Inflammation in Rats

Hong

et al. 2020

Oxidative Medicine and Cellular Longevity

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“…As showed in Figure 2, MgIG improves liver injury induced by various factors, decreases oxidative stress and inflammatory response, normalizes AST, ALT and DBIL levels, and restores liver function (54)(55)(56)(57)(67)(68)(69)(70)(71)163). For kidney injury, MgIG stabilizes the structure of podocytes to reduce proteinuria, pro-inflammatory response and oxidative stress (38,41,75).…”

Section: Improvement Of Multiple Organ Damagementioning

confidence: 95%

“…These results indicate that MgIG may block the further development of the inflammatory response at an early stage of COVID-19. Meanwhile, MgIG significantly decreases NOX1, NOX2 and NOX4 expression (39,45), inhibits ROS and iNOS production, normalizes SOD and MDA level (39,41,45,57,71), therefore, MgIG effectively inhibits oxidative stress response in the body. In terms of mechanism, MgIG may inhibit the activation of inflammation and oxidative pathways, such as TLR4/NF-κB, TGF-β1/Smad, JAK2/STAT3 and p38 MAPK/Akt/ NOX4 signaling pathways (43,45,68).…”

Section: Inhibition Of Cytokine Storm and Oxidative Stressmentioning

confidence: 98%

“…In concanavalin A-induced mouse autoimmune hepatitis model, MgIG (50 or 100 mg/kg ip, qd) can reduce serum AST and ALT levels, inhibit CD4 + CD25 -CD69 + subset proliferation and NLPR3 inflammasome activation to improve autoimmune hepatitis (70). In rat model with acute necrotizing pancreatitis through retrograde injection of 5% sodium taurocholate into the biliary-pancreatic duct, MgIG (30 mg/kg ig, qd) increases liver SOD levels, reduces MDA accumulation, and inhibits IL-1β, and NF-κB, showing its inhibition of oxidative stress and inflammatory response as well as attenuation of liver damage aggravation induced by high fat diet (71).…”

Section: Liver Fibrosis and Othersmentioning

confidence: 99%

“…It reduces serum and hippocampal SOD activity, reduces MDA, TNF-α, IL-6 and IL-1β levels, down-regulates MgIG's effects on various liver diseases and possible mechanisms. MgIG has hepatoprotective properties mainly by inhibiting IL-6 pathway, Hippo/Yap pathway, and ferroptosis pathway, etc (45,57,63,64,(67)(68)(69)71),. and activating ERS pathway and Nrf2 pathway(53,65).…”

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confidence: 99%

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A narrative review of COVID-19: magnesium isoglycyrrhizinate as a potential adjuvant treatment

et al. 2021

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Coronavirus disease 2019 (COVID-19) has become a global pandemic affecting more than 200 countries with 87 million patients worldwide as of January 7, 2021. Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) replicates in a large amount and reaches high-titer levels in a short time after the infection. COVID-19 caused by SARS-CoV-2 shows clinical symptoms mainly including fever, fatigue, dry cough, and dyspnea. In more severe COVID-19 patients, viral pneumonia characterized by bilateral ground glass or patchy opacity, may lead to acute respiratory distress syndrome (ARDS), cytokine storm, multi-organ damage, and even death. Unfortunately, there is no effective therapy for COVID-19 until now.Magnesium isoglycyrrhizinate (MgIG), a magnesium salt of 18-α glycyrrhizic acid stereoisomer, belongs to the fourth generation of glycyrrhizic acid preparation. MgIG has various pharmacological activities including anti-inflammation, anti-oxidation, anti-virus, and immunoregulation, showing the protection against the injury of the vital organs (such as kidney, heart, and lung). Clinically, MgIG injection is usually used as a hepatoprotective agent to treat liver diseases. This narrative review summarizes the research and application of MgIG, and provides the evidence supporting the recommended MgIG as supportive therapy in the "Management Standard for Mild and Common Patients of Coronavirus Disease 2019

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Magnesium in renal fibrosis

et al. 2022

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Magnesium isoglycyrrhizinate alleviates liver injury in obese rats with acute necrotizing pancreatitis

Cited by 14 publications

References 36 publications

High-Fat Diet Aggravates Acute Pancreatitis via TLR4-Mediated Necroptosis and Inflammation in Rats

High-Fat Diet Aggravates Acute Pancreatitis via TLR4-Mediated Necroptosis and Inflammation in Rats

A narrative review of COVID-19: magnesium isoglycyrrhizinate as a potential adjuvant treatment

Magnesium in renal fibrosis

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