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Protective Effect of Polydatin on Jejunal Mucosal Integrity, Redox Status, Inflammatory Response, and Mitochondrial
Hao Zhang1,2,3, Yanan Chen1, Yue Li4
1College of Animal Science & Technology, Nanjing Agricultural University, Nanjing 210095, China.
Insights
Polydatin (PD) supplementation protected piglets with intrauterine growth retardation (IUGR) from intestinal injury by improving gut barrier function and reducing inflammation. This study highlights PD as a potential therapeutic for neonatal gut development issues.
Area of Science:
- Neonatal physiology and developmental biology
- Gastroenterology and nutrition research
- Pharmacology and therapeutic interventions
Background:
- Intrauterine growth retardation (IUGR) significantly impairs neonatal gut development, leading to limited treatment options.
- IUGR-induced intestinal injury is characterized by barrier dysfunction, oxidative stress, and inflammation.
- Effective strategies to mitigate IUGR-related gut damage are crucial for improving neonatal outcomes.
Purpose of the Study:
- To evaluate the protective effects of polydatin (PD) against intestinal injury in piglets with IUGR.
- To investigate PD's impact on gut barrier integrity, oxidative stress, inflammation, and mitochondrial function in IUGR models.
- To determine the therapeutic potential of PD for enhancing neonatal gut development.
Main Methods:
- Utilized a piglet model, comparing intrauterine growth retardation (IUGR) piglets with normal birth weight (NBW) littermates.
- Administered diets supplemented with polydatin (PD) or a basal diet to piglets from 21 to 35 days of age.
- Assessed jejunal damage, bacterial translocation, apoptosis, oxidative stress markers, inflammatory cytokines, and mitochondrial function.
Main Results:
- PD treatment significantly reduced bacterial translocation, circulating diamine oxidase, and D-lactate levels in IUGR piglets.
- PD decreased the apoptotic rate while increasing villus height and the villus height to crypt depth ratio.
- PD enhanced antioxidant enzyme activities, reduced oxidative damage markers, and mitigated inflammatory responses and mitochondrial dysfunction.
Conclusions:
- Polydatin (PD) effectively improves jejunal integrity and barrier function in IUGR piglets.
- PD mitigates mucosal oxidative and immunological damage, suggesting a role in reducing inflammation and stress.
- PD facilitates mitochondrial function and energy production, indicating a comprehensive protective effect on the developing gut.
Abstract:
Intrauterine growth retardation (IUGR) delays the gut development of neonates, but effective treatment strategies are still limited. This study used newborn piglets as a model to evaluate the protective effect of polydatin (PD) against IUGR-induced intestinal injury. In total, 36 IUGR piglets and an equal number of normal birth weight (NBW) littermates were fed either a basal diet or a PD-supplemented diet from 21 to 35 days of age. Compared with NBW, IUGR induced jejunal damage and barrier dysfunction of piglets, as indicated by observable bacterial translocation, enhanced apoptosis, oxidative and immunological damage, and mitochondrial dysfunction. PD treatment decreased bacterial translocation and inhibited the IUGR-induced increases in circulating diamine oxidase activity (P = 0.039) and D-lactate content (P = 0.004). The apoptotic rate (P = 0.024) was reduced by 35.2% in the PD-treated piglets, along with increases in villus height (P = 0.033) and in ratio of villus height to crypt depth (P = 0.049). PD treatment promoted superoxide dismutase (P = 0.026) and glutathione S-transferase activities (P = 0.006) and reduced malondialdehyde (P = 0.015) and 8-hydroxy-2'-deoxyguanosine accumulation (P = 0.034) in the jejunum. The PD-treated IUGR piglets showed decreased jejunal myeloperoxidase activity (P = 0.029) and tumor necrosis factor alpha content (P = 0.035) than those received a basal diet. PD stimulated nuclear sirtuin 1 (P = 0.028) and mitochondrial citrate synthase activities (P = 0.020) and facilitated adenosine triphosphate production (P = 0.009) in the jejunum of piglets. Furthermore, PD reversed the IUGR-induced declines in mitochondrial DNA content (P = 0.048), the phosphorylation of adenosine monophosphate-activated protein kinase alpha (P = 0.027), and proliferation-activated receptor gamma coactivator 1 alpha expression (P = 0.033). Altogether, the results indicate that PD may improve jejunal integrity, mitigate mucosal oxidative and immunological damage, and facilitate mitochondrial function in IUGR piglets.
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