Nephroprotective potential of Panduratin A against colistin-induced renal injury via attenuating mitochondrial dysfunction and cell apoptosis

Worakajit, Nichakorn; Thipboonchoo, Natechanok; Chaturongakul, Soraya; Jutabha, Promsuk; Soontornniyomkij, Virawudh; Tuchinda, Patoomratana; Soodvilai, Sunhapas

doi:10.1016/j.biopha.2022.112732

Cited by 13 publications

(12 citation statements)

References 32 publications

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“…This kidney protective activity is predicted due to panduratin A and/or other constituents contained in the rhizome of this plant. As reported by previous studies, panduratin A attenuated colistin toxicity in human renal proximal tubular cells (RPTEC/TERT1) (22,23) and in mice (23). This compound blocked the activation of ERK1/2 and caspase 3 in cisplatin-treated mice (23).…”

Section: Discussionsupporting

confidence: 77%

The protective effect of Boesenbergia rotunda extract on cisplatin-exposed human embryonic kidney-293 cells by inhibiting the expression of kidney injury molecule-1, neutrophil gelatinase associated-lipocalin, NF-κB, and caspases

Sujana

Saptarini

Sumiwi

et al. 2022

J Herbmed Pharmacol

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Introduction: Acute kidney injury (AKI) is a major problem in platinum-based chemotherapy patients. Boesenbergia rotunda can induce the generation of osteoblast cells and significantly increase pancreatic antioxidant enzyme activities; therefore, this study aimed to investigate the cytotoxicity of cisplatin on human embryonic kidney-293 (HEK-293) cells and the protective impact of the ethanol extract of B. rotunda (EEBR) against such conditions. Methods: Cytotoxicity was assessed using the CCK-8/WST-8 reagent, while the protective activity was assayed on 1 µg/mL cisplatin-exposed HEK-293 cells by quantifying the expression of nephrotoxicity biomarkers, e.g., kidney injury molecule-1 (Kim-1) and neutrophil gelatinase associated-lipocalin (NGAL), nuclear factor-kappaB (NF-κB), apoptotic caspase-3, and caspase-7 genes, in cisplatin-exposed HEK-293 cells. Results: Cisplatin was confirmed as highly toxic against the HEK-293 cells (IC50 = 2.5145 μg/ mL), whereas quercetin was of moderate toxicity (IC50 = 185.6225 μg/mL). EEBR revealed an IC50 = 40.0655 μg/mL. Moreover, EEBR concentrations of 5, 10, and 20 µg/mL confirmed its remarkable protective activity against cisplatin-exposed HEK-293 cells (P=0.031, 0.014, 0.046, respectively) compared to the cisplatin-treated cell lines without treatment. The quantitative real-time polymerase chain reaction (PCR) revealed that a higher concentration of EEBR significantly suppressed the expression of Kim-1, while lower concentrations of EEBR significantly inhibited NGAL and NF-κB genes. Higher concentrations of EEBR reduced the expression of caspase-3. All concentrations of EEBR stimulated the expression of caspase-7. Conclusion: The significant protective activity observed in this study indicated that EEBR might be beneficial in protecting kidney cells against cisplatin.

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Section: Discussionsupporting

confidence: 77%

The protective effect of Boesenbergia rotunda extract on cisplatin-exposed human embryonic kidney-293 cells by inhibiting the expression of kidney injury molecule-1, neutrophil gelatinase associated-lipocalin, NF-κB, and caspases

Sujana

Saptarini

Sumiwi

et al. 2022

J Herbmed Pharmacol

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“…In addition, the cisplatin-resistant ovarian cancer cell line model also exhibited apoptosis via intrinsic and extrinsic mechanisms incorporating p53 alterations [ 176 ]. Bcl-2 family proteins’ expression abnormality and upregulation of apoptosis inhibitors that block the effect of caspases and stabilize the mitochondrial permeability pore [ 177 , 178 ]. Our study evaluated the apoptotic effect on sciatic nerve BCL-2 associated x immunohistochemical examination for the normal control group that showed negative expression of BCL-2 in sciatic nerve fibers.…”

Section: Resultsmentioning

confidence: 99%

Sustainable Release of Propranolol Hydrochloride Laden with Biconjugated-Ufasomes Chitosan Hydrogel Attenuates Cisplatin-Induced Sciatic Nerve Damage in In Vitro/In Vivo Evaluation

et al. 2022

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Peripheral nerve injuries significantly impact patients’ quality of life and poor functional recovery. Chitosan–ufasomes (CTS–UFAs) exhibit biomimetic features, making them a viable choice for developing novel transdermal delivery for neural repair. This study aimed to investigate the role of CTS–UFAs loaded with the propranolol HCl (PRO) as a model drug in enhancing sciatica in cisplatin-induced sciatic nerve damage in rats. Hence, PRO–UFAs were primed, embedding either span 20 or 60 together with oleic acid and cholesterol using a thin-film hydration process based on full factorial design (24). The influence of formulation factors on UFAs’ physicochemical characteristics and the optimum formulation selection were investigated using Design-Expert® software. Based on the optimal UFA formulation, PRO–CTS–UFAs were constructed and characterized using transmission electron microscopy, stability studies, and ex vivo permeation. In vivo trials on rats with a sciatic nerve injury tested the efficacy of PRO–CTS–UFA and PRO–UFA transdermal hydrogels, PRO solution, compared to normal rats. Additionally, oxidative stress and specific apoptotic biomarkers were assessed, supported by a sciatic nerve histopathological study. PRO–UFAs and PRO–CTS–UFAs disclosed entrapment efficiency of 82.72 ± 2.33% and 85.32 ± 2.65%, a particle size of 317.22 ± 6.43 and 336.12 ± 4.9 nm, ζ potential of −62.06 ± 0.07 and 65.24 ± 0.10 mV, and accumulatively released 70.95 ± 8.14% and 64.03 ± 1.9% PRO within 6 h, respectively. Moreover, PRO–CTS–UFAs significantly restored sciatic nerve structure, inhibited the cisplatin-dependent increase in peripheral myelin 22 gene expression and MDA levels, and further re-established sciatic nerve GSH and CAT content. Furthermore, they elicited MBP re-expression, BCL-2 mild expression, and inhibited TNF-α expression. Briefly, our findings proposed that CTS–UFAs are promising to enhance PRO transdermal delivery to manage sciatic nerve damage.

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“…Consistent with our study, previous investigations have reported that mechanistically, colistin-induced nephrotoxicity is mainly on mitochondrial dysfunction triggered by oxidative stress (5,18). Moreover, the bene cial effects of antioxidant and mitochondria protective agents such as panduratin A, melatonin, ascorbic acid and baicalein on colistin-induced nephrotoxicity, shows the importance of mitochondrial damage and oxidative stress in induction of kidney damage by this drug (14,(32)(33)(34). It has been reported that mitochondrial dysfunction and oxidative stress are important contributory factors to the lysosomal damages (35).…”

Section: Discussionmentioning

confidence: 99%

“…AIF-M2 has NADH-Q oxidoreductase activity which can be the target of colistin in mitochondria (12). There are several studies that show mitochondrial dysfunction is associated with nephrotoxicity caused by the colistin (4,(12)(13)(14). It seems that inhibiting mitochondrial dysfunction or replacing the damaged mitochondria via increasing the number of mitochondria ( ssion and fusion) and mitochondrial transplantation can be a suitable approach to reduce the nephrotoxicity caused by colistin.…”

Section: Introductionmentioning

confidence: 99%

Transplantation of Healthy Mitochondria into Rat Renal Proximal Tubular Cells Reduces Colistin- Induced Mitochondrial Dysfunction and Cellular Damage: An In Vitro Study

Arjmand

Mohammadabadi

Faizi

et al. 2023

Preprint

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Background Kidney damage caused by colistin (polymyxin E) can bring about a decrease in creatinine clearance, potential proteinuria, cylindruria and oliguria in treated patients. It is therefore imperative to develop a new therapeutic strategy for reducing kidney damage after treatment with colistin. Mitochondrial damage is one of contributing factors in colistin-induced nephrotoxicity. Given the therapeutic benefits of mitochondrial transplantation by exogenous healthy mitochondria, we hypothesized that this strategy would be capable of ameliorating renal proximal tubular cells damage following exposure with colistin.Methods For this purpose, we isolated rat renal proximal tubular cells (RPTCs) form kidney and exposed them with toxic concertation of colistin with/without rat healthy isolated mitochondria for 4 hours. Cellular parameters such as lactate dehydrogenase (LDH), reactive oxygen species (ROS) formation, mitochondrial membrane potential (MMP), caspase 3 activation, lysosomal damage, glutathione and ATP content were measured.Results The results showed that administration of isolated mitochondria could improve colistin-induced nephrotoxicity and reduce mitochondrial dysfunction. Exogenous mitochondria reduced the activity of LDH, production of ROS, ATP and GSH depletion, loss of MMP, lysosomal damages and cell death.Conclusion To the best of our knowledge, these results provide the first direct experimental evidence that mitochondrial transplantation is capable of ameliorating cellular damage following treatment with colistin. These findings support that mitochondrial transplantation can be a promising therapeutic strategy for colistin-associated mitochondrial dysfunction and kidney damage.

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Nephroprotective potential of Panduratin A against colistin-induced renal injury via attenuating mitochondrial dysfunction and cell apoptosis

Cited by 13 publications

References 32 publications

The protective effect of Boesenbergia rotunda extract on cisplatin-exposed human embryonic kidney-293 cells by inhibiting the expression of kidney injury molecule-1, neutrophil gelatinase associated-lipocalin, NF-κB, and caspases

The protective effect of Boesenbergia rotunda extract on cisplatin-exposed human embryonic kidney-293 cells by inhibiting the expression of kidney injury molecule-1, neutrophil gelatinase associated-lipocalin, NF-κB, and caspases

Sustainable Release of Propranolol Hydrochloride Laden with Biconjugated-Ufasomes Chitosan Hydrogel Attenuates Cisplatin-Induced Sciatic Nerve Damage in In Vitro/In Vivo Evaluation

Transplantation of Healthy Mitochondria into Rat Renal Proximal Tubular Cells Reduces Colistin- Induced Mitochondrial Dysfunction and Cellular Damage: An In Vitro Study

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