Evaluation of Both Free Radical Scavenging Capacity and Antioxidative Damage Effect of Polydatin

Jin, Ju; Li, Yan; Zhang, Xiuli; Chen, Tongsheng; Wang, Yifei; Wang, Zhiping

doi:10.1007/978-3-319-38810-6_8

Cited by 18 publications

(14 citation statements)

References 8 publications

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“…The presence of inflammatory processes in mNSCLC patients may be related to the presence of malignancy itself, to concomitant smoke-associated bronchopulmonary chronic disease and to the presence of relapsing bacterial infections related to incomplete integrity the airways (44)(45)(46)(47)(48)(49).…”

Section: Discussionmentioning

confidence: 99%

Inflammatory Markers and Procalcitonin Predict the Outcome of Metastatic Non-Small-Cell-Lung-Cancer Patients Receiving PD-1/PD-L1 Immune-Checkpoint Blockade

Nardone¹,

Giannicola

Bianco

et al. 2021

Front. Oncol.

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Peripheral-immune-checkpoint blockade (P-ICB) with mAbs to PD-1 (nivolumab and pembrolizumab) or PD-L1 (atezolizumab, durvalumab, avelumab) alone or combination with chemotherapy represents a novel active treatment for mNSCLC patients. However, this therapy can be associated to immune-related adverse events (irAEs) and high cost. Therefore, finding reliable biomarkers of response and irAEs is strongly encouraged to accurately select patients who may potentially benefit from the immuno-oncological treatment. This is a retrospective multi-institutional analysis performed on ninety-five mNSCLC patients who received real-world salvage therapy with nivolumab or atezolizumab between December 2015 and April 2020. The outcome of these patients in term of PFS and OS was evaluated in comparison with different serum levels of C-reactive protein (CRP), Erythrocyte Sedimention Rate (ESR) and Procalcitonin (PCT) by performing Kaplan–Meier and Log-rank test and multivariate analysis. We found that high baseline levels of CRP, ESR, and PCT were strongly predictive of poor outcome (P <0.05) with the worse prognosis detected in those patients with a baseline levels of both ESR and PCT over the pre-established cut off (median OS recorded in patients with no marker over the cut off vs. those with just one marker over the cut off vs. those with both markers over the cut off: 40 ± 59 vs. 15.5 ± 5.5 vs. 5.5 ± 1.6 months, respectively; P <0.0001). Our results suggest the predictive value of systemic inflammation and suggest a potential role of PCT in predicting a poor outcome in mNSCLC receiving PD-1/PD-L1 blocking mAbs. This finding also suggests a potential role of subclinical bacterial infections in defining the response to PD-1/PD-L1 blocking mAbs that deserves further and more specific investigations.

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Section: Discussionmentioning

confidence: 99%

Inflammatory Markers and Procalcitonin Predict the Outcome of Metastatic Non-Small-Cell-Lung-Cancer Patients Receiving PD-1/PD-L1 Immune-Checkpoint Blockade

Nardone¹,

Giannicola

Bianco

et al. 2021

Front. Oncol.

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“…Among which, the 4′-hydroxyl group is the preferred reaction site as a result of the resonance effects that occur between the two aromatic rings [ 40 – 42 ]. Therefore, PD can quench a variety of free radicals produced both in vitro and in vivo , including 2,2-diphenyl-1-picryl-hydrazyl, 2,2-azobis (2-amidino-propane) dihydrochloride, superoxide anion, hydrogen peroxide, and hydroxyl radicals [ 27 , 43 , 44 ]. Notably, Fabris et al [ 45 ] showed that PD is a suitable compound for the prevention and control of the lipid peroxidation because of its lipophilicity.…”

Section: Discussionmentioning

confidence: 99%

Protective Effect of Polydatin on Jejunal Mucosal Integrity, Redox Status, Inflammatory Response, and Mitochondrial Function in Intrauterine Growth-Retarded Weanling Piglets

Zhang

Chen

2020

Oxidative Medicine and Cellular Longevity

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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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“…These properties provide PD better bioavailability than resveratrol. PD retains powerful free radical scavenging property, and also exhibits anti‐oxidant functions . PD was also shown to exert cardioprotective effects against ischemia/reperfusion injury .…”

Section: Introductionmentioning

confidence: 99%

Polydatin alleviated radiation‐induced lung injury through activation of Sirt3 and inhibition of epithelial–mesenchymal transition

Cao

Xiao

Liu

et al. 2017

J Cellular Molecular Medi

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Radiation‐induced lung injury (RILI) is one of the most common and fatal complications of thoracic radiotherapy. It is characterized with two main features including early radiation pneumonitis and fibrosis in later phase. This study was to investigate the potential radioprotective effects of polydatin (PD), which was shown to exert anti‐inflammation and anti‐oxidative capacities in other diseases. In this study, we demonstrated that PD‐mitigated acute inflammation and late fibrosis caused by irradiation. PD treatment inhibited TGF‐β1‐Smad3 signalling pathway and epithelial–mesenchymal transition. Moreover, radiation‐induced imbalance of Th1/Th2 was also alleviated by PD treatment. Besides its free radical scavenging capacity, PD induced a huge increase of Sirt3 in culture cells and lung tissues. The level of Nrf2 and PGC1α in lung tissues was also elevated. In conclusion, our data showed that PD attenuated radiation‐induced lung injury through inhibiting epithelial–mesenchymal transition and increased the expression of Sirt3, suggesting PD as a novel potential radioprotector for RILI.

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Evaluation of Both Free Radical Scavenging Capacity and Antioxidative Damage Effect of Polydatin

Cited by 18 publications

References 8 publications

Inflammatory Markers and Procalcitonin Predict the Outcome of Metastatic Non-Small-Cell-Lung-Cancer Patients Receiving PD-1/PD-L1 Immune-Checkpoint Blockade

Inflammatory Markers and Procalcitonin Predict the Outcome of Metastatic Non-Small-Cell-Lung-Cancer Patients Receiving PD-1/PD-L1 Immune-Checkpoint Blockade

Protective Effect of Polydatin on Jejunal Mucosal Integrity, Redox Status, Inflammatory Response, and Mitochondrial Function in Intrauterine Growth-Retarded Weanling Piglets

Polydatin alleviated radiation‐induced lung injury through activation of Sirt3 and inhibition of epithelial–mesenchymal transition

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