ArticleBMC gastroenterology2024
Vitamin B6 ameliorates acute pancreatitis by suppressing the caspase3 signaling pathway.
Article in BMC gastroenterology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Cell death and its interaction with mitochondrial dysfunction in pathogenesis of acute pancreatitis: a comprehensive review.Apoptosis : an international journal on programmed cell death · 2026Review
- Genome Mining for Hub Genes Related to Endoplasmic Reticulum Stress in Pancreatitis: A Perspective from In Silico Characterization.Molecular biotechnology · 2026Article
- Serum aberrant expression of miR-331-3p and its diagnostic value in severe pancreatitis.BMC gastroenterology · 2026Article
- The role and interplay among Autophagy, Apoptosis, and ferroptosis in acute pancreatitis: mechanisms and therapeutic approaches.Molecular biology reports · 2025Review
- Multifaceted role of the vitamin B6 pathway in cancer: metabolism, immune interaction, and temporal and spatial regulation.Genes & development · 2025Review
- Pretreatment withFrontiers in pharmacology · 2025Article
- Targeting the programmed cell death signaling mechanism with natural products for the treatment of acute pancreatitis: a review.Frontiers in pharmacology · 2025Review
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAcute pancreatitis (AP) is a prevalent exocrine inflammatory disorder of the pancreas characterized by pancreatic inflammation and injury to acinar cells. Vitamin B6 (VB6) is a vital nutrient that plays a significant role in preserving human health and has anti-inflammatory and anti-apoptotic effects.
methodsThis study aimed to explore the potential pancreatic protective effects of VB6 in mitigating pancreatic inflammation and apoptosis induced by taurocholate sodium (TLCS) in an AP model and to assess the underlying mechanism of action. AP was induced in Sprague‒Dawley (SD) rats through TLCS administration and lipopolysaccharide (LPS)-treated AR42J cells, followed by treatment with VB6.
resultsVarious parameters associated with AP were assessed in both plasma and pancreatic tissues. VB6 has been shown to ameliorate the severity of AP through various mechanisms. It effectively reduces the levels of serum amylase, lipase, and inflammatory factors, thereby mitigating histological injury to the pancreas. Moreover, VB6 inhibited pancreatic apoptosis by downregulating bax expression and up-regulating Bcl2 expression in TLCS-treated rats. Additionally, VB6 suppressed the expression of caspase3. The anti-inflammatory and anti-apoptotic effects of VB6 observed in LPS-treated AR42J cells are consistent with those observed in a rat model of AP.
conclusionsThese results suggest that VB6 exerts anti-inflammatory and anti-apoptotic effects through inhibition of the caspase3 signaling pathway and has a protective effect against AP.
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