Protective Effects of Polyenoylphosphatidylcholine in Rats With Severe Acute Pancreatitis

Li, Xiangyi; Wu, Zheng; Sha, Huanchen; Wang, Zheng; Ma, Zhenhua; Wu, Erxi; Ma, Qingyong

doi:10.1097/mpa.0000000000000292

Cited by 3 publications

(2 citation statements)

References 32 publications

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“…Nonetheless, Van Antwerpen et al [43] in their in vitro study showed that captopril, by inhibiting the MPO/HOCl system, was able to significantly reduce the oxidative modification of low-density lipoprotein in a dosedependent manner. Furthermore, Li et al [44] demonstrated that pathological injury of the lung in rats with intense acute pancreatitis was decreased with captopril treatment.…”

Section: Discussionmentioning

confidence: 99%

Captopril protects against burn-induced cardiopulmonary injury in rats

Sağlam¹,

Şehirli²,

Özdamar³

et al. 2014

Ulus Travma Acil Cerrahi Derg

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Section: Discussionmentioning

confidence: 99%

Captopril protects against burn-induced cardiopulmonary injury in rats

Sağlam¹,

Şehirli²,

Özdamar³

et al. 2014

Ulus Travma Acil Cerrahi Derg

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show abstract

“…Therefore, early diagnosis is of great importance in patients with AP. Emerging studies provide evidence that pancreatitis leads to severe pathological changes in pancreatic acinar cells, and the damage of cells promotes the release of enzymes and organelles, which resulted in the occurrence of SAP [5]. Thus, strategies to promote pancreatic acinar cell apoptosis may have therapeutic potential in the treatment of AP.…”

Section: Introductionmentioning

confidence: 99%

Dysregulation of miR-192-5p in acute pancreatitis patients with nonalcoholic fatty liver and its functional role in acute pancreatitis progression

2020

Bioscience Reports

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Background: Nonalcoholic fatty liver disease (NAFLD) is a frequent metabolic disease and has been demonstrated to contribute to the severity of acute pancreatitis (AP). The present study aimed to investigate the aberrant expression of microRNA-192-5p (miR-192-5p) in AP patients with NAFLD, and further analyze the clinical significance and biological function of miR-192-5p in AP progression. Methods: Expression of miR-192-5p was estimated using quantitative real-time PCR (qRT-PCR). Diagnostic value of miR-192-5p was evaluated by the receiver operating characteristic curve (ROC). The effects of miR-192-5p on cell proliferation, apoptosis and inflammatory response of pancreatic acinar cells were further assessed by CCK-8 assay, flow cytometry and enzyme-linked immunosorbent assay (ELISA). Results: Circulating miR-192-5p was decreased in AP patients with NAFLD compared with those patients without NAFLD and healthy controls (P<0.05). The down-regulated expression of miR-192-5p had a relative high diagnostic accuracy to distinguish the AP patients with NAFLD from the cases without NAFLD. Furthermore, the overexpression of miR-192-5p in pancreatic acinar cells led to the decreased cell proliferation, increased cell apoptosis and suppressed inflammatory reaction (all P<0.05). Conclusion: Collectively, all data indicated that serum expression of miR-192-5p in AP patients with NAFLD is significantly decreased and serves as a candidate diagnostic biomarker. The up-regulation of miR-192-5p in pancreatic acinar cell leads to increased cell apoptosis and decreased inflammatory response, suggesting the potential of miR-192-5p as a therapeutic target of AP.

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TM6SF2 E167K variant decreases PNPLA3-mediated PUFA transfer to promote hepatic steatosis and injury in MASLD

Sun,

Ding,

Tan

et al. 2024

Clin Mol Hepatol

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Backgrounds/Aims: Transmembrane 6 superfamily member 2 (TM6SF2) E167K variant is closely associated with the occurrence and development of metabolic dysfunction-associated steatotic liver disease (MASLD). However, the role and mechanism of TM6SF2 E167K variant during MASLD progression are not yet fully understood.Methods: The Tm6sf2167K knock-in (KI) mice were subjected to high-fat diet (HFD). Hepatic lipid levels of Tm6sf2167K KI mice were detected by lipidomics analysis. Thin-layer chromatography (TLC) was used to measure the newly synthesized triglyceride (TG) and phosphatidylcholine (PC).Results: The TM6SF2 E167K variant significantly aggravated hepatic steatosis and injury in HFD-induced mice. Decreased polyunsaturated PC level and increased polyunsaturated TG level were found in liver tissue of HFDinduced Tm6sf2167K KI mice. Mechanistic studies demonstrated that the TM6SF2 E167K variant increased the interaction between TM6SF2 and PNPLA3, and impaired PNPLA3-mediated transfer of polyunsaturated fatty acids (PUFAs) from TG to PC. The TM6SF2 E167K variant increased the level of fatty acid-induced malondialdehyde and reactive oxygen species, and decreased fatty acid-downregulated cell membrane fluidity. Additionally, the TM6SF2 E167K variant decreased the level of hepatic PC containing C18:3, and dietary supplementation of PC containing C18:3 significantly attenuated the TM6SF2 E167K-induced hepatic steatosis and injury in HFD-fed mice.Conclusions: The TM6SF2 E167K variant could promote its interaction with PNPLA3 and inhibit PNPLA3-mediated transfer of PUFAs from TG to PC, resulting in the hepatic steatosis and injury during MASLD progression. PC containing C18:3 could act as a potential therapeutic supplement for MASLD patients carrying the TM6SF2 E167K variant.

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Protective Effects of Polyenoylphosphatidylcholine in Rats With Severe Acute Pancreatitis

Abstract: Polyenoylphosphatidylcholine could reduce the damage to the pancreas through increasing pancreatic acinar cell membrane fluidity and pancreatic tissue calcium pump activity. Polyenoylphosphatidylcholine also scavenges oxygen free radicals and reduces lipid peroxide levels.

Cited by 3 publications

References 32 publications

Captopril protects against burn-induced cardiopulmonary injury in rats

Captopril protects against burn-induced cardiopulmonary injury in rats

Dysregulation of miR-192-5p in acute pancreatitis patients with nonalcoholic fatty liver and its functional role in acute pancreatitis progression

TM6SF2 E167K variant decreases PNPLA3-mediated PUFA transfer to promote hepatic steatosis and injury in MASLD

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