Unique Triterpenoid of Jujube Root Protects Cisplatin-induced Damage in Kidney Epithelial LLC-PK1 Cells via Autophagy Regulation

Lee, Dahae; Kang, Kyo Bin; Kim, Hyun Woo; Park, Jung Sik; Hwang, Gwi Seo; Kang, Ki Sung; Choi, Seung-Ho; Yamabe, Noriko; Kim, Ki‐Hyun

doi:10.3390/nu12030677

Cited by 11 publications

(8 citation statements)

References 36 publications

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“…However, we are aware that our research may exist some limitations compared to previous reports at the same scope. Firstly, the effect of muscone on other cell death pathways caused by cisplatin including autophagy [ 32 ] and nuclear factor-κB activation [ 33 ] has not been investigated yet in this study. Secondly, the experimental results are just at in vitro scope.…”

Section: Resultsmentioning

confidence: 99%

Preventive Effect of Muscone against Cisplatin Nephrotoxicity in LLC-PK1 Cells

et al. 2020

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Cisplatin, one of the most common antitumor agents, is widely applied to treat various cancerous diseases and is included in the World Health Organization Model List of Essential Medicines. Cisplatin therapy is used to treat 10–20% of all cancerous cases, and its cure rate is especially high in testicular cancer (over 90%). However, a major side effect of this anticancer drug is nephrotoxicity, limiting treatment effect and reducing the quality of life in cancer patients. Muscone, an odoriferous constituent of musk, was confirmed to inhibit cisplatin-induced LLC-PK1 kidney proximal tubule cell death in a dose-dependent manner. In term of renal protective mechanism, muscone inhibited cisplatin oxidative toxicity by decreasing reactive oxygen species (ROS) level and stimulating HO-1 expression. Muscone also exerted anti-inflammation effect through inhibition of p38 phosphorylation. Furthermore, muscone mitigated cisplatin-induced apoptosis in LLC-PK1 cells via both intrinsic and extrinsic pathways by inhibiting pro-apoptotic protein Bax expression, and cleaved caspase-3, 7, and 8; and increase of anti-apoptotic protein Bcl-2 level. In addition, the anti-apoptotic effect of muscone also was enhanced by preventing p53 expression and its phosphorylation. Our study showed that muscone may be a potential protective agent against cisplatin-induced nephrotoxicity.

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Section: Resultsmentioning

confidence: 99%

Preventive Effect of Muscone against Cisplatin Nephrotoxicity in LLC-PK1 Cells

et al. 2020

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“…In addition, however, we have added alternative therapies gleaned from our 17 years of experience, such as zizyphus jujube, black seed oil, probiotics, pumpkin seeds, walking barefoot, and sweat therapy, all of which are beneficial in CKD. It has been reported that jujube fruits have beneficial effects for the prevention of hypertension, kidney damage, oxidative stress, and inflammation, and they also can help to decrease anxiety and depression [ 18 , 19 ]. We have also shown that jujube can aid in the control of dyslipidemia and diabetes in CKD patients [ 20 ].…”

Section: Discussionmentioning

confidence: 99%

Discontinuation of Hemodialysis After 8 Years in Favor of Toprak’s Kidney Care in a Patient with End-Stage Kidney Disease

et al. 2021

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Patient: Male, 77-year-old Final Diagnosis: End-stage renal failure Symptoms: No symptoms Medication:— Clinical Procedure: — Specialty: Nephrology Objective: Unusual clinical course Background: End-stage kidney disease patients who need hemodialysis for more than 3 months are less likely to be able to discontinue dialysis. Patient care, however, can play a role in improving kidney function. In this study, we showed that even a patient on hemodialysis for 8 years can discontinue or reduce the number of weekly dialysis sessions through kidney care. Here, we report the effect of patient care on the ability to cease dialysis or reduce dialysis sessions, discuss such cessation or reduction in chronic hemodialysis patients, and describe proper follow-up procedure for a patient whose dialysis has been discontinued or reduced. Case Report: Here, we present a 77-year-old man who had undergone hemodialysis 3 times weekly for 75 months, after which dialysis sessions were gradually decreased and terminated within 21 months while undergoing Toprak’s Kidney Care, a kidney care program. The patient went without dialysis for 10 months. Then, hemodialysis was started once weekly for 46 months, as the glomerular filtration rate values decreased significantly. Following this period, he underwent hemodialysis 3 times weekly for 19 months. During these follow-up periods, 2 hospitalizations were required due to pneumonia and atrial fibrillation. There were no major adverse cardiac events. The patient is still in our follow-up care. Conclusions: Gradual termination of an 8-year period of hemodialysis through a kidney care program without kidney transplantation is very rare. In end-stage kidney disease patients with adequate urination, kidney care should be considered to terminate hemodialysis or reduce the weekly dialysis sessions.

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“…Trichostatin A and SAHA (broadspectrum HDAC inhibitors) and Tubastatin A (HDAC6 specific inhibitor) also protects against cisplatin nephrotoxicity in kidneys through AMPK-mTOR pathways but sensitizes cancer cells to cisplatin cytotoxicity by enhancing DNA damage [113,114,[160][161][162]. In addition, some natural products, neferine [95,163], emodin [164,165], ginsenoside Rb3 [97], oridonin [98], 3DC2ME [166], scutellarin [167,168], and rottlerin [49,112] also exert the same effect through AKT/ mTOR pathways. Of interest, trehalose regulates autophagy by rapid and transient lysosomal enlargement and membrane permeabilization (LMP) through TFEB, but does not induce mTOR [129,169].…”

Section: Activation Of Autophagymentioning

confidence: 99%

Autophagy in Cisplatin Nephrotoxicity during Cancer Therapy

Wen

et al. 2021

Cancers

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Cisplatin is a widely used chemotherapeutic agent but its clinical use is often limited by nephrotoxicity. Autophagy is a lysosomal degradation pathway that removes protein aggregates and damaged or dysfunctional cellular organelles for maintaining cell homeostasis. Upon cisplatin exposure, autophagy is rapidly activated in renal tubule cells to protect against acute cisplatin nephrotoxicity. Mechanistically, the protective effect is mainly related to the clearance of damaged mitochondria via mitophagy. The role and regulation of autophagy in chronic kidney problems after cisplatin treatment are currently unclear, despite the significance of research in this area. In cancers, autophagy may prevent tumorigenesis, but autophagy may reduce the efficacy of chemotherapy by protecting cancer cells. Future research should focus on developing drugs that enhance the anti-tumor effects of cisplatin while protecting kidneys during cisplatin chemotherapy.

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Unique Triterpenoid of Jujube Root Protects Cisplatin-induced Damage in Kidney Epithelial LLC-PK1 Cells via Autophagy Regulation

Cited by 11 publications

References 36 publications

Preventive Effect of Muscone against Cisplatin Nephrotoxicity in LLC-PK1 Cells

Preventive Effect of Muscone against Cisplatin Nephrotoxicity in LLC-PK1 Cells

Discontinuation of Hemodialysis After 8 Years in Favor of Toprak’s Kidney Care in a Patient with End-Stage Kidney Disease

Autophagy in Cisplatin Nephrotoxicity during Cancer Therapy

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