Attenuation of cyclosporine A induced nephrotoxicity by schisandrin B through suppression of oxidative stress, apoptosis and autophagy

Lai, Qiao; Luo, Zhengzhong; Wu, Chun-Ying; Lai, Sisi; Wei, Hanmei; Li, Tongming; Wang, Qing; Yu, Yang

doi:10.1016/j.intimp.2017.08.019

Cited by 43 publications

(32 citation statements)

References 32 publications

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“…There is evident renal congestion with aggregation of inflammatory cells in the renal tissue. These findings coincide with the previously published results by Lassila et al .,[15] Wu et al .,[16] Lai et al .,[17] and confirmed recently by El-Bassossy and Eid. [2]…”

Section: Discussionsupporting

confidence: 94%

“…Mitochondrial and endoplasmic stress is implicated in the pathogenesis of CSA-induced renal impairment. [1728] CSA therapy is specifically reported to induce reactive oxygen species production in renal mesangial cells[29] as well as it is also implicated in reducing renal antioxidant defense mechanism. These findings clarify the role of oxidative stress in medicating CSA-induced nephrotoxicity[27] which comes in agreement with the result of the current study.…”

Section: Discussionmentioning

confidence: 99%

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Renal oxidative stress and inflammatory response in perinatal Cyclosporine-A exposed rat progeny and its relation to gender

El-Bassossy

Hassanien

Bima

et al. 2019

J Microsc Ultrastruct

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Background and Aim of the Work: The current study postulated that cyclosporine A (CSA) could induce gender-specific renal damage. Hence, the current study aims to investigate the nephrotoxic effect of perinatal exposure of male and female rat progeny to CSA. Moreover, it aims to evaluate the oxidative stress and inflammation as a possible pathophysiologic mechanism. Materials and Methods: Female rats were randomly allocated to two groups of four and assigned to undergo either CSA (15 mg/kg/day; the 6 th day after conception and continuing until the progeny were weaned) or vehicle treatment as control groups. At the age of 6 weeks, the progeny were divided into the following four groups: male progeny of control-group mothers (M-vehicle, 7); male progeny of CSA-treated mothers (M-CSA, 9); female progeny of control-group mothers (F-vehicle, 7); and female progeny of CSA-treated mothers (F-CSA, 6). Serum adiponectin, tumor necrosis factor-α (TNF-α) and creatinine, creatinine clearance, and urinary 8-isoprostane were measured. Histopathological examination by hematoxylin and eosin stain of Kidney was carried out. Results: Proteinuria and decreased creatinine clearance are significant in M-CSA than M-vehicle and F-CSA. 8-isoprostane is lower in F-CSA than F-vehicle. Increased TNF-α and decreased adiponectin levels in M-CSA than M-vehicle were observed. No significant differences were found in female rat groups. Conclusion: From the current study, it could be concluded that CSA could induce renal inflammation as well as oxidative stress that may explain the impaired renal function. The sex difference was a prominent finding in their vulnerability to CSA effects.

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Section: Discussionsupporting

confidence: 94%

Section: Discussionmentioning

confidence: 99%

Renal oxidative stress and inflammatory response in perinatal Cyclosporine-A exposed rat progeny and its relation to gender

El-Bassossy

Hassanien

Bima

et al. 2019

J Microsc Ultrastruct

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“…Lycopene, known to play an antioxidant role, ameliorated atrazine-induced nephrotoxicity by upregulating Nrf2, AMPK, and autophagic flux, as well as by decreasing oxidative stress and p62 levels [167]. Schisandrin B, isolated from the fruit of Schisandra chinensis , provided a protective role in cyclosporine (CsA)-induced nephrotocxicity, attenuated CsA-induced nephrotoxicity by activating Nrf2, preventing ROS accumulation and oxidative stress, and allowed recovery of CsA-induced blockade of autophagic flux [168]. Cyclic helix B peptide, a tissue-protective peptide mimicking the 3D structure of erythropoietin, which has been reported to ameliorate IR [169], protected HK-2 cells from H 2 O 2 -induced injury through activation of the Nrf2 signaling pathway and autophagy [170].…”

Section: Ros-mediated Regulation Of Autophagy and Its Impact In Kimentioning

confidence: 99%

Molecular Interactions Between Reactive Oxygen Species and Autophagy in Kidney Disease

Kaushal

Chandrashekar

Juncos

2019

IJMS

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Reactive oxygen species (ROS) are highly reactive signaling molecules that maintain redox homeostasis in mammalian cells. Dysregulation of redox homeostasis under pathological conditions results in excessive generation of ROS, culminating in oxidative stress and the associated oxidative damage of cellular components. ROS and oxidative stress play a vital role in the pathogenesis of acute kidney injury and chronic kidney disease, and it is well documented that increased oxidative stress in patients enhances the progression of renal diseases. Oxidative stress activates autophagy, which facilitates cellular adaptation and diminishes oxidative damage by degrading and recycling intracellular oxidized and damaged macromolecules and dysfunctional organelles. In this review, we report the current understanding of the molecular regulation of autophagy in response to oxidative stress in general and in the pathogenesis of kidney diseases. We summarize how the molecular interactions between ROS and autophagy involve ROS-mediated activation of autophagy and autophagy-mediated reduction of oxidative stress. In particular, we describe how ROS impact various signaling pathways of autophagy, including mTORC1-ULK1, AMPK-mTORC1-ULK1, and Keap1-Nrf2-p62, as well as selective autophagy including mitophagy and pexophagy. Precise elucidation of the molecular mechanisms of interactions between ROS and autophagy in the pathogenesis of renal diseases may identify novel targets for development of drugs for preventing renal injury.

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“…As one of the major active ingredients in Schisandra chinensis, Sch B has been extensively studied for its diverse pharmacological effects (18). Previous studies have demonstrated that Sch B has potent antioxidant and cytoprotective effects against different types of oxidative stress-induced cell injury in hepatocytes (19)(20)(21), cardiomyocytes (22,23), neurcyte (24,25), kidney tubule cells (26) and trophoblasts (27). In most of these cell types, the antioxidant effects of Sch B derive from Nrf2 activation and subsequent upregulation of antioxidant enzyme expression.…”

Section: Introductionmentioning

confidence: 99%

Schisandrin B protects human keratinocyte-derived HaCaT�cells from tert-butyl hydroperoxide-induced oxidative damage through activating the Nrf2 signaling pathway

et al. 2018

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Schisandrin B (Sch B), an active extract of Schisandra chinensis, has demonstrated antioxidant activity in a number of in vitro and in vivo models. In the present study, the capacity of Sch B to protect against oxidative injury in keratinocytes using the human keratinocyte-derived HacaT cell line was investigated. To induce oxidative injury, tert-Butyl hydroperoxide (tBHP) was employed. The results indicate that Sch B efficiently reduced tBHP-induced cell death, reactive oxygen species (ROS) generation, protein oxidation, lipid peroxidation and dNA damage. Sch B also effectively attenuated the loss of mitochondrial membrane potential (MMP), and restored adenosine triphosphate (ATP) levels in tBHP-injured HacaT cells. Furthermore, Sch B enhanced the expression of key antioxidant enzymes, including catalase, heme oxygenase-1, glutathione peroxidase, and superoxide dismutase, and further engaged the nuclear factor-erythroid 2-related factor 2 (Nrf2) signaling pathway by modulating its phosphorylation through activating multiple upstream kinases, including protein kinase B, adenosine monophosphate-activated protein kinase and mitogen-activated protein kinases (MAPKs). The present study suggests that Sch B provides a protective effect in keratinocytes in response to oxidative injury via reinforcing the endogenous antioxidant defense system. Therefore, it may be applied as an adjuvant therapy or in health foods to delay the skin aging process and the onset of skin diseases caused by oxidative stress.

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Attenuation of cyclosporine A induced nephrotoxicity by schisandrin B through suppression of oxidative stress, apoptosis and autophagy

Cited by 43 publications

References 32 publications

Renal oxidative stress and inflammatory response in perinatal Cyclosporine-A exposed rat progeny and its relation to gender

Renal oxidative stress and inflammatory response in perinatal Cyclosporine-A exposed rat progeny and its relation to gender

Molecular Interactions Between Reactive Oxygen Species and Autophagy in Kidney Disease

Schisandrin B protects human keratinocyte-derived HaCaT�cells from tert-butyl hydroperoxide-induced oxidative damage through activating the Nrf2 signaling pathway

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