Protective effect of syringic acid on kidney ischemia-reperfusion injury

Sancak, Eyüp Burak; Akbaş, Alpaslan; Silan, Coşkun; Çakır, Dilek Ülker; Türkön, Hakan; Özkanli, Sıdıka Şeyma

doi:10.3109/0886022x.2016.1149868

Cited by 32 publications

(17 citation statements)

References 27 publications

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“…Tokmak et al (10) reported that SA pretreatment in spinal cord I/R reduced oxidative stress and neuronal degeneration. SA also attenuated renal I/R injury (11). However, the role of SA in myocardial I/R injury remains to be elucidated.…”

Section: Introductionmentioning

confidence: 97%

Syringic acid inhibits apoptosis pathways via downregulation of p38MAPK and JNK signaling pathways in H9c2 cardiomyocytes following hypoxia/reoxygenation injury

Ding

Wang

Guo

et al. 2017

Molecular Medicine Reports

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Syringic acid (SA), a naturally occur-ring O‑methy-lated trihydroxybenzoic acid monomer extracted from Dendrobium nobile Lindl., has been demonstrated to attenuate renal ischemia‑reperfusion (I/R) injury. However, the role of SA in myocardial I/R injury is unclear. The present study aimed to clarify the cardioprotective effect of SA in myocardial I/R injury in vitro and explore the potential molecular mechanisms. In the present study, it was revealed that pretreatment with SA increased the viability and inhibited oxidant stress in H9c2 cardiomyocytes that had suffered hypoxia/reoxygenation (H/R). SA also markedly downregulated B‑cell lymphoma 2 (Bcl‑2) expression and inhibited the expression of Bcl‑2‑like protein 4 (Bax) and cleaved caspase‑3 in H9c2 cardiomyocytes induced by H/R. In addition, SA significantly alleviated H/R-induced the phosphorylation of p38 mitogen‑activated protein kinase (p38MAPK) and c‑Jun N‑terminal kinase (JNK) in H9c2 cardiomyocytes. In conclusion, the present study demonstrated that SA inhibits the apoptosis of H9c2 cardiomyocytes following H/R injury via reduced activation of the p38MAPK and JNK signaling pathways. The results support the therapeutic usage of SA in the treatment of myocardial infarction.

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Section: Introductionmentioning

confidence: 97%

Syringic acid inhibits apoptosis pathways via downregulation of p38MAPK and JNK signaling pathways in H9c2 cardiomyocytes following hypoxia/reoxygenation injury

Ding

Wang

Guo

et al. 2017

Molecular Medicine Reports

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“…A study by Ilhan et al determined that HBO therapy attenuated MDA levels by increasing SOD and GPx activities in rats with renal ischemia reperfusion ( 6 ). In recent years, diverse oxidant species can be measured totally and lipid peroxidation activities have been analyzed by evaluating TOS ( 23 ). The protecting enzymes from oxidative stress of SOD, catalase (CAT), glutathione reductase (GR) and glutathione peroxidase (GPx) resist the destructive actions of ROS, and these enzymes engender the TAC.…”

Section: Discussionmentioning

confidence: 99%

“…The advantage of TAC measurement is that it can measure the antioxidant capacity of all antioxidants in a biological sample. Even more importantly, the ratio of TOS to TAC is accepted as the OSI, which is a more valuable indicator to reflect oxidative status than TAC or TOS level alone ( 13 , 23 ). In this study, we found that tissue MDA, TOS and OSI levels were significantly higher in the UPUO group than in the Sham group.…”

Section: Discussionmentioning

confidence: 99%

Attenuation of partial unilateral ureteral obstruction – induced renal damage with hyperbaric oxygen therapy in a rat model

et al. 2017

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Objective:The objective of the present study was to evaluate the effectiveness of HBO therapy on biochemical parameters, renal morphology and renal scintigraphy in rats undergoing chronic unilateral partial ureteral obstruction (UPUO).Material and methods:Thirty-five rats were divided into five equal groups: Control group; Sham group; HBO group; UPUO group and UPUO/HBO group. The effects of HBO therapy were examined using biochemical parameters and histopathological changes. After calculating the score for each histopathological change, the total histopathological score was obtained by adding all the scores. In addition, dynamic renal scintigraphy findings were evaluated.Results:Serum parameters indicating inflammation, serum tumor necrosis factor- alpha, ischemia modified-albumin, IMA/albumin ratio and Pentraxin-3 levels, were observed to be high in the UPUO group and low in the UPUO/HBO treatment group. Similarly, in the treatment group, the reduction in malondialdehyde, total oxidant status and oxidative stress index levels and increase in total antioxidant capacity values were observed to be statistically significant compared to the UPUO group (p<0.001, p=0.007, p<0.001, p=0.001, respectively). The total score and apoptosis index significantly decreased after administration of HBO treatment. Dynamic 99mTc-MAG3 renal scintigraphy also showed convincing evidence regarding the protective nature of HBO against kidney injury. In the UPUO/HBO therapy group, the percentage contribution of each operated kidney increased significantly compared to the UPUO group (41.73% versus 32.72%).Conclusion:The findings of this study indicate that HBO therapy had a reno-protective effect by reducing inflammation and oxidative stress, and preserving renal function after renal tissue damage due to induction of UPUO.

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“…and apoptosis in rat renal ischemia-reperfusion injury have all been shown to be inhibited by pre-treatment or treatment with Syra (8)(9)(10). However, to date, the effect of Syra on nP cells and their apoptosis is unknown, although these aforementioned studies could suggest that this molecule might reverse the apoptosis of nP cells.…”

Section: Gene Expression Profile Of Lipopolysaccharide-induced Apoptomentioning

confidence: 99%

Gene expression profile of lipopolysaccharide‑induced apoptosis of nucleus pulposus cells reversed by syringic acid

et al. 2020

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apoptosis of nucleus pulposus (nP) cells has an important role in the process of intervertebral disc degeneration (idd), and the search for novel compounds to prevent apoptosis from occurring is urgently required. in the present study, syringic acid (Syra) was found to exhibit no cytotoxicity on nP cells, and was able to reverse the cytotoxicity, as well as the abnormal expression of Bcl-2 and caspase-3, that were induced by lipopolysaccharide (lPS). The transcriptomes of each group were then analyzed using rna-Seq. a total of 65 differentially expressed genes (deGs) were identified in LPS-stimulated groups (lPS group vs. control group), 819 DEGs were identified in the SyrA-reversed groups (Syra plus lPS group vs. lPS group), and a further 25 deGs were identified in the Syra plus lPS group compared with the control group. reverse transcription-quantitative Pcr validation indicated that the alterations in expression of uroplakin 3B-like 1 (uPK3Bl1), voltage-dependent calcium channel subunit α-2/δ-1 (cacna2d1) and polo-like kinase 4 (PlK4) were consistent with the corresponding results of rna-Seq, and that these genes were involved in both lPS-stimulation and Syra-reversion processes. Kyoto encyclopedia of Genes and Genomes analyses indicated that the deGs in Syra-reversed groups were involved in, amongst other pathways, 'autophagy-other' and 'apoptosis-multiple species'. in conclusion, the addition of Syra to the nP cells co-incubated with lPS appeared to help prevent the abnormal expression of mrnas and apoptosis that had been identified in nP cells incubated with lPS alone. The potential mechanism underlying the reversion of Syra might be attributed to the regulation of cacna2d1 and PlK4.

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Protective effect of syringic acid on kidney ischemia-reperfusion injury

Cited by 32 publications

References 27 publications

Syringic acid inhibits apoptosis pathways via downregulation of p38MAPK and JNK signaling pathways in H9c2 cardiomyocytes following hypoxia/reoxygenation injury

Syringic acid inhibits apoptosis pathways via downregulation of p38MAPK and JNK signaling pathways in H9c2 cardiomyocytes following hypoxia/reoxygenation injury

Attenuation of partial unilateral ureteral obstruction – induced renal damage with hyperbaric oxygen therapy in a rat model

Gene expression profile of lipopolysaccharide‑induced apoptosis of nucleus pulposus cells reversed by syringic acid

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