Sinapic acid alleviates cisplatin-induced acute kidney injury by mitigating oxidative stress and apoptosis

Altındağ, Fikret; Ergen, Hidayet

doi:10.1007/s11356-022-22940-x

Cited by 6 publications

(6 citation statements)

References 44 publications

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“…The current study has shown that the TAA inoculation in rats caused severe hepatotoxic damage and the SA treatment revealed the significant suppressing effect of this liver damage as shown through histopathological (H & E), reduced Masson's Trichrome stains, and up-regulated the HSP 70 immunostain, indicating its hepatoprotection actions. Similarly, studies have shown the SA potentials in the positive modulation of the HSP 70 protein expression in different rat experiments [9,48] The endogenous antioxidant enzymes in the homogenized hepatic tissues are considered significant indicators of oxidative stress-related liver damage [49]. The present data revealed that rats treated with only TAA had significantly lower liver antioxidant enzymes (SOD and CAT) than that found in control rats.…”

Section: Discussionsupporting

confidence: 62%

“…Sinapic acid (family: phenylpropanoid) is a natural derivative of hydroxycinnamic acid that has been known for composing various bioactivities, anti-inflammatory, antiradical, and antitumor actions [8,9]. Recent Studies revealed that SA and its derivatives (syringic acid) exhibit significant anti-inflammatory and anti-radical potentials in chemical-induced kidney and liver injuries in rats [8,10].…”

Section: Introductionmentioning

confidence: 99%

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Sinapic Acid Attenuate Liver Injury by Modulating Antioxidant Activity and Inflammatory Cytokines in Thioacetamide-Induced Liver Cirrhosis in Rats

Jabbar,

Alamri,

Abdulla

et al. 2023

Biomedicines

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Sinapic acid (SA) is a natural pharmacological active compound found in berries, nuts, and cereals. The current study aimed to investigate the protective effects of SA against thioacetamide (TAA) fibrosis in rats by histopathological and immunohistochemical assays. The albino rats (30) were randomly divided into five groups (G). G1 was injected with distilled water 3 times/week and fed orally daily with 10% Tween 20 for two months. G2–5 were injected with 200 mg/kg TAA three times weekly for two months and fed with 10% Tween 20, 50 mg/kg silymarin, 20, and 40 mg/kg of SA daily for 2 months, respectively. The results showed that rats treated with SA had fewer hepatocyte injuries with lower liver index (serum bilirubin, total protein, albumin, and liver enzymes (ALP, ALT, and AST) and were similar to that of control and silymarin-treated rats. Acute toxicity for 2 and 4 g/kg SA showed to be safe without any toxic signs in treated rats. Macroscopic examination showed that hepatotoxic liver had an irregular, rough surface with micro and macro nodules and histopathology expressed by Hematoxylin and Eosin, and Masson Trichrome revealed severe inflammation and infiltration of focal necrosis, fibrosis, lymphocytes, and proliferation bile duct. In contrast, rats fed with SA had significantly lower TAA toxicity in gross and histology and liver tissues as presented by less liver tissue disruption, lesser fibrosis, and minimum in filtered hepatocytes. Immunohistochemistry of rats receiving SA showed significant up-regulation of HSP 70% and down-regulation of alpha-smooth muscle actin (α-SMA) protein expression compared to positive control rats. The homogenized liver tissues showed a notable rise in the antioxidant enzymes (SOD and CAT) actions with significantly lower malondialdehyde (MDA) levels compared to that of the positive control group. Furthermore, the SA-treated rats had significantly lower TNF-a, IL-6, and higher IL-10 levels than the positive control rats. Thus, the findings suggest SA as a hepatoprotective compound due to its inhibitory effects on fibrosis, hepatotoxicity, liver cell proliferation, up-regulation of HSP 70, and downregulation of α-SMA expression, inhibiting lipid peroxidation (MDA), while retaining the liver index and antioxidant enzymes to normal.

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Section: Discussionsupporting

confidence: 62%

Section: Introductionmentioning

confidence: 99%

Sinapic Acid Attenuate Liver Injury by Modulating Antioxidant Activity and Inflammatory Cytokines in Thioacetamide-Induced Liver Cirrhosis in Rats

Jabbar,

Alamri,

Abdulla

et al. 2023

Biomedicines

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“…After 1 h, normal saline was injected intraperitoneally. This was performed once a day for three days [ 2 ]; CP group: rats were injected with CP (dissolved in DMF, 7 mg/kg, S1166, Selleck, MA, USA) intraperitoneally on the first day, and after 1 h, they were injected with normal saline once a day for 3 days [ 3 , 23 ]; CP + Dex 10 μg/kg group: rats were injected with CP (dissolved in DMF, 7 mg/kg) intraperitoneally on the first day, and 1 h later, Dex (dissolved in normal saline, 10 μg/kg, 145108-58-3, Sigma, MO, USA) was injected intraperitoneally, and the injection of Dex was performed once a day for three consecutive days [ 4 , 24 ]; CP + Dex 25 μg/kg group: a single intraperitoneal injection of CP (7 mg/kg) was administered to rats on the first day, and after 1 h, Dex (25 μg/kg) was injected intraperitoneally once a day for three consecutive days [ 25 ]. Rats were euthanized 96 h after CP injection, and kidney tissue and peripheral blood were collected.…”

Section: Methodsmentioning

confidence: 99%

“…Subsequently, kidney tissues in the control, CP, CP + Dex 10 μg/kg, and CP + Dex 25 μg/kg groups were observed under an optical microscope, and renal tubule injury scored at the same time according to Altındağ et al. [ 23 ].…”

Section: Methodsmentioning

confidence: 99%

Mechanism of dexmedetomidine protection against cisplatin induced acute kidney injury in rats

Zheng,

Ma,

Luo

et al. 2024

Renal Failure

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Objective This study explored the molecular mechanisms by which dexmedetomidine (Dex) alleviates cisplatin (CP)-induced acute kidney injury (AKI) in rats. Methods CP-induced AKI models were established, and Dex was intraperitoneally injected at different concentrations into rats in the model groups. Subsequently, rats were assigned to the control, CP, CP + Dex 10 μg/kg, and CP + Dex 25 μg/kg groups. After weighing the kidneys of the rats, the kidney arterial resistive index was calculated, and CP-induced AKI was evaluated. In addition, four serum biochemical indices were measured: histopathological damage in rat kidneys was detected; levels of inflammatory factors, interleukin (IL)-1β, IL-18, IL-6, and tumor necrosis factor alpha, in kidney tissue homogenate of rats were assessed through enzyme-linked immunosorbent assay (ELISA); and levels of NLRP-3, caspase-1, cleaved caspase-1, gasdermin D (GSDMD), and GSDMD-N in kidney tissues of rats were determined via western blotting. Results Dex treatment reduced nephromegaly and serum clinical marker upregulation caused by CP-induced AKI. In addition, hematoxylin and eosin staining revealed that Dex treatment relieved CP-induced kidney tissue injury in AKI rats. ELISA analyses demonstrated that Dex treatment reduced the upregulated levels of proinflammatory cytokines in the kidney tissue of AKI rats induced by CP, thereby alleviating kidney tissue injury. Western blotting indicated that Dex alleviated CP-induced AKI by inhibiting pyroptosis mediated by NLRP-3 and caspase-1. Conclusion Dex protected rats from CP-induced AKI, and the mechanism may be related to NLRP-3/Caspase-1-mediated pyroptosis.

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“…15 SNP is a phenolic compound effective in the prevention of lipid peroxidation and has antioxidant, anti-inflammatory, antiapoptotic, anticancer and antihyperglycaemic properties. 16 We hypothesize that SNP may ameliorate oxidative stress and associated damages in PbAc-induced lung toxicity based on all of this scientific evidence. Therefore, this study aimed to determine the efficacy of SNP in Pb-induced lung toxicity.…”

mentioning

confidence: 94%

Sinapic acid protects against lead acetate‐induced lung toxicity by reducing oxidative stress, apoptosis, inflammation, and endoplasmic reticulum stress damage

Akaras,

Kucukler,

Gur

et al. 2024

Environmental Toxicology

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Lead acetate (PbAc) is a compound that produces toxicity in many tissues after exposure. Sinapic acid (SNP) possesses many biological and pharmacological properties. This study aimed to investigate the efficacy of SNP on the toxicity of PbAc in lung tissue. PbAc was administered orally at 30 mg/kg and SNP at 5 or 10 mg/kg for 7 days. Biochemical, genetic, and histological methods were used to investigate inflammatory, apoptotic, endoplasmic reticulum stress, and oxidative stress damage levels in lung tissue. SNP administration induced PbAc‐reduced antioxidant (GSH, SOD, CAT, and GPx) and expression of HO‐1 in lung tissue. It also reduced MDA, induced by PbAc, and thus alleviated oxidative stress. SNP decreased the inflammatory markers NF‐κB, TNF‐α and IL‐1β levels induced by PbAc in lung tissue and exhibited anti‐inflammatory effect. PbAc increased apoptotic Bax, Apaf‐1, and Caspase‐3 mRNA transcription levels and decreased anti‐apoptotic Bcl‐2 in lung tissues. SNP decreased apoptotic damage by reversing this situation. On the other hand, SNP regulated these markers and brought them closer to the levels of the control group. PbAc caused prolonged ER stress by increasing the levels of ATF6, PERK, IRE1α, GRP78 and this activity was stopped and tended to retreat with SNP. After evaluating all the data, While PbAc caused toxic damage in lung tissue, SNP showed a protective effect by reducing this damage.

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Sinapic acid alleviates cisplatin-induced acute kidney injury by mitigating oxidative stress and apoptosis

Cited by 6 publications

References 44 publications

Sinapic Acid Attenuate Liver Injury by Modulating Antioxidant Activity and Inflammatory Cytokines in Thioacetamide-Induced Liver Cirrhosis in Rats

Sinapic Acid Attenuate Liver Injury by Modulating Antioxidant Activity and Inflammatory Cytokines in Thioacetamide-Induced Liver Cirrhosis in Rats

Mechanism of dexmedetomidine protection against cisplatin induced acute kidney injury in rats

Sinapic acid protects against lead acetate‐induced lung toxicity by reducing oxidative stress, apoptosis, inflammation, and endoplasmic reticulum stress damage

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