Determinants and outcomes of acute pancreatitis in patients hospitalized for COVID-19: Early pandemic experience

Aldiabat, Mohammad; Kilani, Yassine; Arshad, Iqra; Rana, Tabeer; Aleyadeh, Wesam; Al Ta'ani, Omar; Aljabiri, Yazan; Alsakarneh, Saqr; Abdelfattah, Thaer; Alhuneafat, Laith; Manvar, Amar

doi:10.1016/j.pan.2023.10.012

Cited by 2 publications

(1 citation statement)

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“…Acute pancreatitis (AP) is a frequent reason for emergency department visits 1 . While mild to moderate forms of AP is associated with self-limiting systemic inflammatory responses in over two-thirds of cases, severe acute pancreatitis (SAP) continues to be a critical illness that requires protracted hospitalization, prolonged time spent in intensive care, and a sluggish recovery process 2,3 .…”

Section: Introductionmentioning

confidence: 99%

Emodin: an alveolar macrophage protector in acute pancreatitis induced lung injury

Chen,

Dong,

Song

et al. 2024

Preprint

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Emodin (EMO), an anthraquinone derivative from roots and leaves of various plants, has been widely used in many inflammatory diseases. Alveolar macrophages (AMs) play a critical role in maintaining alveolar homeostasis in the lung. To investigate the pathophysiological mechanism of AMs in acute pancreatitis-associated lung injury (AP-ALI) and the potential protective therapeutic of EMO for AP-ALI, AMs isolated from AP-ALI mice, murine cell line MH-S and RAW264.7 were pre-treated with EMO to assess its protective roles on regulating inflammation, pyroptosis, and mitophagy of macrophages in AP-ALI. The results showed that 1) in vivo, the relative quantity of AMs was significantly decreased across the time in API-ALI; however, the mitochondria flux presented earlier changes than the resident AMs alteration in our experimental system. EMO pretreatment significantly alleviated the severity of lung injury and improved the damaged alveolar structure, and further reversed the reduction of mitochondria impairment in AMs in mice. 2) In vitro, EMO significantly suppressed LPS/ATP associated NLRP3 inflammasome activation, enhanced mitophagy, and protected mitochondria damage. Furthermore, the data of mitophagy inhibition by 3-MA demonstrated that EMO protective effects were partially via manipulating mitophagy-mitochondria-alveolar macrophage axis. Our data shed light on the comprehensive understanding on EMO therapeutics in AP-ALI.

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Section: Introductionmentioning

confidence: 99%