Protective effects of sinapic acid against lead acetate-induced nephrotoxicity: a multi-biomarker approach

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Antimicrobial agent resistance has become a growing health issue across the world. Colistin (COL) is one of the drugs used in the treatment of multidrug‐resistant bacteria resulting in toxic effects. Naringin (NRG), a natural flavonoid, has come to the fore as its antioxidant, anti‐inflammatory, and antiapoptotic activities. The aim of the present study was to determine whether NRG has protective effects on COL‐induced toxicity in testicular tissue. Thirty‐five male Spraque rats were randomly divided into five groups (n = 7 per group): Control, COL, NRG, COL + NRG 50, COL + NRG 100. COL (15 mg/kg b.w., i.p., once per/day), and NRG (50 or 100 mg/kg, oral, b.w./once per/day) were administered for 7 days. The parameters of oxidative stress, inflammation, apoptosis, and autophagic damage were evaluated by using biochemical, molecular, western blot, and histological methods in testicular issues. NRG treatment reversed the increased malondialdehyde level and reduced antioxidants (superoxide dismutase, catalase, glutathione peroxidase, and glutathione) levels due to COL administration (p < 0.001), and oxidative stress damage was mitigated. Nuclear factor erythroid 2‐related factor‐2 pathway, one of the antioxidant defence systems, was stimulated by NRG (p < 0.001). NRG treatment reduced the levels of markers for the pathways of apoptotic (p < 0.001) and autophagic (p < 0.001) damages induced by COL. Sperm viability and the live/dead ratio were reduced by COL but enhanced by NRG treatment. Testicular tissue integrity was damaged by COL but showed a tendency to improve by NRG. In conclusion, COL exhibited toxic effect on testicular tissue by elevating the levels of oxidative stress, apoptosis, autophagy, inflammation, and tissue damage. NRG demonstrated a protective effect by alleviating toxic damage.

Protective effects of naringin on colistin‐induced damage in rat testicular tissue: Modulating the levels of Nrf‐2/HO‐1, AKT‐2/FOXO1A, Bax/Bcl2/Caspase‐3, and Beclin‐1/LC3A/LC3B signaling pathways

Kankılıç,

Şimşek,

Akaras

et al. 2024

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Naringin protects against paclitaxel‐induced toxicity in rat testicular tissues by regulating genes in pro‐inflammatory cytokines, oxidative stress, apoptosis, and JNK/MAPK signaling pathways

Kankılıç,

Küçükler,

Gür

et al. 2024

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Paclitaxel (PTX), which is actively used in the treatment of many types of cancer, has a toxic effect by causing increased oxidative stress in testicular tissues. Naringin (NRG) is a natural flavonoid found in plants, and its antioxidant properties are at the forefront. This study aims to investigate the protective feature of NRG in PTX‐induced testicular toxicity.Thirty‐five male Sprague rats were divided into five groups: control, NRG, PTX, PTX + NRG50, and PTX + NRG100. Rats were administered PTX (2 mg/kg, BW) intraperitoneally once daily for the first 5 days. Then, between the 6th and 14th days, NRG (50 and 100 mg/kg) was administered orally once a day.NRG reduced PTX‐induced lipid peroxidation and increased testicular tissue antioxidant capacity (superoxide dismutase, catalase, glutathione peroxidase, and glutathione). While NRG reduces the mRNA expression levels of nuclear factor kappa B, tumor necrosis factor‐alpha, interleukin‐1 beta, cyclooxygenase‐2, interleukin‐6, inducible‐nitric oxide synthase, mitogen‐activated protein kinase 14 (MAPK)14, MAPK15, c‐Jun N‐terminal kinase, P53, Apaf1, Caspase3, Caspase6, Caspase9, and Bax in testicular tissues; it caused an increase in Nrf2, HO‐1, NQO1 and Bcl‐2 levels. NRG also improved the structural and functional integrity of testicular tissue disrupted by PTX. PTX‐induced sperm damage was alleviated by NRG.NRG showed a protective effect by alleviating the PTX‐induced testicular toxicity by increasing oxidative stress, inflammation, apoptosis, and autophagy.

The ameliorative effect of carvacrol on sodium arsenite‐induced hepatotoxicity in rats: Possible role of Nrf2/HO‐1, RAGE/NLRP3, Bax/Bcl‐2/Caspase‐3, and Beclin‐1 pathways

Gencer,

Gür,

İleritürk

et al. 2024

Arsenic is a toxic environmental pollutant heavy metal, and one of its critical target tissues in the body is the liver. Carvacrol is a natural phytocompound that stands out with its antioxidant, anti‐inflammatory, and antiapoptotic properties. The current study aims to investigate the protective feature of carvacrol against sodium arsenite‐induced liver toxicity. Thirty‐five Sprague‐Dawley male rats were divided into five groups: Control, Sodium arsenite (SA), CRV, SA + CRV25, and SA + CRV50. Sodium arsenite was administered via oral gavage at a dose of 10 mg/kg for 14 days, and 30 min later, CRV 25 or 50 mg/kg was administered via oral gavage. Oxidative stress, inflammation, apoptosis, autophagy damage pathways parameters, and liver tissue integrity were analyzed using biochemical, molecular, western blot, histological, and immunohistological methods. Carvacrol decreased sodium arsenite‐induced oxidative stress by suppressing malondialdehyde levels and increasing superoxide dismutase, catalase, glutathione peroxidase activities, and glutathione levels. Carvacrol reduced inflammation damage by reducing sodium arsenite‐induced increased levels of NF‐κB and the cytokines (TNF‐α, IL‐1β, IL‐6, RAGE, and NLRP3) it stimulates. Carvacrol also reduced sodium arsenite‐induced autophagic (Beclin‐1, LC3A, and LC3B) and apoptotic (P53, Apaf‐1, Casp‐3, Casp‐6, Casp‐9, and Bax) parameters. Carvacrol preserved sodium arsenite‐induced impaired liver tissue structure. Carvacrol alleviated toxic damage by reducing sodium arsenite‐induced increases in oxidative stress, inflammation, apoptosis, and autophagic damage parameters in rat liver tissues. Carvacrol was also beneficial in preserving liver tissue integrity.