Modulatory effects of carvacrol against cadmium-induced hepatotoxicity and nephrotoxicity by molecular targeting regulation

Kandemir, Fatih Mehmet; Çağlayan, Cüneyt; Darendelioğlu, Ekrem; Küçükler, Sefa; İzol, Ebubekir; Kandemir, Özge

doi:10.1016/j.lfs.2021.119610

Cited by 39 publications

(30 citation statements)

References 61 publications

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“…Flavonoids, which are secondary metabolites of plants, are phenolic compounds found in almost all vegetables and fruits 18–21 . Flavonoids are compounds with various biological and pharmacological properties, including anti‐allergic, vasodilator, anti‐inflammatory, antiapoptotic, antioxidant, and antithrombotic 22–24 .…”

Section: Introductionmentioning

confidence: 99%

Evaluation of protective effects of quercetin against cypermethrin‐induced lung toxicity in rats via oxidative stress, inflammation, apoptosis, autophagy, and endoplasmic reticulum stress pathway

İleritürk

Kandemir

2022

Environmental Toxicology

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Cypermethrin (CYP), a type II synthetic pyrethroid, is the most widely used insecticide worldwide. Inhalation of it may cause side effects. This study is aimed to examine potential protection of quercetin (QUE) which is a well-known antioxidant in CYPinduced lung toxicity. Accordingly, 35 Spraque Dawley male rats were divided into five equal groups as follows: I-Control group, II-QUE group (50 mg/kg/b.w. QUE), III-CYP group (25 mg/kg/b.w. CYP), IV-CYP + QUE 25 (25 mg/kg/b.w. CYP + 25 mg/ kg/b.w. QUE), V-CYP + QUE (25 mg/kg/b.w. CYP + 50 mg/kg/b.w. QUE) were treated with oral gavage throughout 28 days. CYP intoxication was associated with increased malondialdehyde level while glutathione concentration, activities of glutathione peroxidase, superoxide dismutase, and catalase reduced. CYP adminisitration caused of apoptosis in the lung by up-regulating caspase-3 and Bax levels and down-regulating Bcl-2. CYP also caused of endoplasmic reticulum (ER) stress by increasing mRNA transcript levels of PERK, IRE1, ATF6, and GRP78. Additionally, it was observed that CYP administration activated IL-6/JAK2/STAT3/MAPK14 signaling pathway and levels of IL-1β, NF-κB, TNF-α, and iNOS in the lung tissue. Therefore, it was determined that CYP administration triggered autophagy by upregulating LC3A and LC3B mRNA transcript levels. Moreover, the protein levels of NF-κB, caspase-3, Bax, Bcl-2, and cytochorme-c were examined by Western blot analysis. However, cotreatment with QUE at a dose of 25 and 50 mg/kg considerably protective oxidative stress, inflammation, apoptosis, ER stress, autophagy, and IL-6/JAK2/STAT3/MAPK14 signaling pathway in lung tissue. Overall, the findings of this study suggest that lung damage associated with CYP toxicity could be protected by QUE administration.

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Section: Introductionmentioning

confidence: 99%

Evaluation of protective effects of quercetin against cypermethrin‐induced lung toxicity in rats via oxidative stress, inflammation, apoptosis, autophagy, and endoplasmic reticulum stress pathway

İleritürk

Kandemir

2022

Environmental Toxicology

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“…In line with these results, previous studies have demonstrated deterioration of renal function in cadmium‐intoxicated rats. [ 32,50 ] Interestingly, this study highlighted the ability of galangin to downregulate KIM‐1, reduce both serum creatinine and BUN, and suppress histopathological abnormalities, underscoring the nephroprotective activity of galangin against cadmium‐evoked nephrotoxicity.…”

Section: Discussionmentioning

confidence: 67%

“…[22,69] Cadmium also depletes the critical nonenzymatic antioxidant GSH and inhibits the antioxidant enzymes, disrupting the cellular redox homeostasis. [25,50] Disruption of the redox balance triggers oxidative damage to the cellular important biomolecules including membrane lipids and DNA. [20,50] Consistent with these studies, this study showed the ability of cadmium to largely deplete GSH, reduce the activity of GSH-related enzymes GCL and GSR, reduce the activity of the antioxidant enzymes CAT and GPx, and diminish TAC in the renal tissues (Figure 3).…”

Section: Discussionmentioning

confidence: 99%

“…[25,50] Disruption of the redox balance triggers oxidative damage to the cellular important biomolecules including membrane lipids and DNA. [20,50] Consistent with these studies, this study showed the ability of cadmium to largely deplete GSH, reduce the activity of GSH-related enzymes GCL and GSR, reduce the activity of the antioxidant enzymes CAT and GPx, and diminish TAC in the renal tissues (Figure 3). In the same context, levels of the oxidative DNA damage marker (8-Oxo-dG), lipid peroxidation markers, and protein oxidation marker PCC were efficiently increased (Figure 2).…”

Section: Discussionmentioning

confidence: 99%

“…Doses of galangin and cadmium chloride were in accordance with previous studies. [41,49,50] Cadmium chloride and galangin were procured from Sigma-Aldrich.…”

Section: Animals and Experimental Designmentioning

confidence: 99%

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Galangin attenuates cadmium‐evoked nephrotoxicity: Targeting nucleotide‐binding domain‐like receptor pyrin domain containing 3 inflammasome, nuclear factor erythroid 2‐related factor 2, and nuclear factor kappa B signaling

Salama

Abd‐Allah

Gad

et al. 2022

J Biochem & Molecular Tox

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The kidney is highly vulnerable to cadmium‐evoked oxidative injury. Galangin is a natural flavone with reported antioxidant properties. This study investigated the potential modulating activity of galangin against cadmium‐induced nephrotoxicity and explored the underlining mechanisms. Western blot analysis, spectrophotometric, ELISA, and histopathological techniques were employed. The results revealed that galangin suppressed tubular injury and improved glomerular function in the cadmium‐intoxicated rats as evidenced by downregulation of kidney injury molecule‐1, serum creatinine, and blood urea nitrogen. Galangin reduced cadmium‐evoked inflammatory response and oxidative stress as indicated by reduced levels of interleukin‐1 beta and TNF‐α, decreased DNA damage, and improved antioxidant potential of the renal tissues. Mechanistically, galangin suppressed the nucleotide‐binding domain‐like receptor pyrin domain containing 3 inflammasome and efficiently decreased caspase‐1 activity in the cadmium‐intoxicated rats. Equally important, it inhibited the cadmium‐induced nuclear translocation of nuclear factor kappa B and upregulated nuclear factor erythroid 2‐related factor 2 signaling. The results highlight the ability of galangin to attenuate cadmium‐evoked nephrotoxicity and support its therapeutic implementation although clinical investigations are warranted.

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18β‐Glycyrrhetinic acid exerts cardioprotective effects against BPA‐induced cardiotoxicity through antiapoptotic and antioxidant mechanisms

Bayav,

Darendelioğlu,

Caglayan

2024

J Biochem & Molecular Tox

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Bisphenol A (BPA) is a synthetic environmental pollutant widely used in industry, as well as is an endocrine disrupting chemicals and has a toxic effects on heart tissue. The aim of this study is to reveal the cardioprotective effects of 18β‐glycyrretinic acid (GA) against BPA‐induced cardiotoxicity in rats. In this study, 40 male rats were used and five different groups (each group includes eight rats) were formed. The rats were applied BPA (250 mg/kg b.w.) alone or with GA (50 and 100 mg/kg b.w.) for 14 days. Rats were killed on Day 15 and heart tissues were taken for analysis. GA treatment decreased serum lactate dehydrogenase and creatine kinase MB levels, reducing BPA‐induced heart damage. GA treatment showed ameliorative effects against lipid peroxidation and oxidative stress caused by BPA by increasing the antioxidant enzyme activities (glutathione peroxidase, superoxide dismutase, and catalase) and GSH level of the heart tissue and decreasing the MDA level. In addition, GA showed antiapoptotic effect by increasing Bcl‐2, procaspase‐3, and ‐9 protein expression levels and decreasing Bax, cytochrome c, and P53 protein levels in heart tissue. As a result, it was found that GA has cardioprotective effects on heart tissue by exhibiting antioxidant and antiapoptotic effects against heart damage caused by BPA, an environmental pollutant. Thus, it was supported that GA could be a potential cardioprotective agent.

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Modulatory effects of carvacrol against cadmium-induced hepatotoxicity and nephrotoxicity by molecular targeting regulation

Cited by 39 publications

References 61 publications

Evaluation of protective effects of quercetin against cypermethrin‐induced lung toxicity in rats via oxidative stress, inflammation, apoptosis, autophagy, and endoplasmic reticulum stress pathway

Evaluation of protective effects of quercetin against cypermethrin‐induced lung toxicity in rats via oxidative stress, inflammation, apoptosis, autophagy, and endoplasmic reticulum stress pathway

Galangin attenuates cadmium‐evoked nephrotoxicity: Targeting nucleotide‐binding domain‐like receptor pyrin domain containing 3 inflammasome, nuclear factor erythroid 2‐related factor 2, and nuclear factor kappa B signaling

18β‐Glycyrrhetinic acid exerts cardioprotective effects against BPA‐induced cardiotoxicity through antiapoptotic and antioxidant mechanisms

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