Apigenin protects from hepatorenal damage caused by lead acetate in rats

Fehaid, Alaa; Al-Ghamdi, Mohammad S.; Alzahrani, Khalid J.; Theyab, Abdulrahman; Al‐Amer, Osama; Al-Shehri, Saad S.; Algahtani, Mohammad; Oyouni, Atif Abdulwahab A.; Alnfiai, Mrim M.; Aly, Mohamed; Alsharif, Khalaf F.; Albrakati, Ashraf; Kassab, Rami B.; Althagafi, Hussam Awwadh E.; Alharthi, Fahad; Moneim, Ahmed E. Abdel; Lokman, Maha S.

doi:10.1002/jbt.23275

Cited by 5 publications

(2 citation statements)

References 47 publications

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“…Furthermore, CoAN is a crucial factor so that an agent can selectively kill tumor cells but with a protective effect on normal tissues. Interestingly, flavonoids have differential effects on normal and tumor tissues [ 46 , 47 , 48 , 49 , 50 , 51 , 52 , 53 , 54 , 55 , 56 , 57 , 58 , 59 , 60 , 61 ]. For instance, Api has been associated with a reduced risk of diabetes.…”

Section: Discussionmentioning

confidence: 99%

Synergism Antiproliferative Effects of Apigenin and Naringenin in NSCLC Cells

et al. 2023

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Non-small cell lung cancer (NSCLC) is one of the leading cancer killers. Apigenin (Api) and Naringenin (Nar) are natural bioactive substances obtained in various vegetables and fruits, possessing anti-tumor effects across multiple studies. This study investigated the latent synergistic antiproliferative functions of Api and Nar in A549 and H1299 NSCLC cells. Cell viability was determined after incubating with different concentrations of Api, Nar, or the combination of Api and Nar (CoAN) for 24 h. Analysis using the CompuSyn software revealed that the CI value of each combined dose was < 1, depicting that the two drugs had a synergistic inhibitory effect. The CoAN (A:N = 3:2) group with the lowest CI value was selected for subsequent experiments. The IC50 of CoAN (A:N = 3:2) was used to determine the cell cycle, the expression ratio of Bax to Bcl2, Caspase 3 activity, and mitochondrial function to assess oxidative stress and apoptosis. The results established that CoAN treatment caused significant cytotoxicity with cell cycle arrest at G2/M phases. Furthermore, CoAN significantly enhanced mitochondria dysfunction, elevated oxidative stress, and activated the apoptotic pathway versus Api or Nar alone groups. Thus, the CoAN chemotherapy approach is promising and deserves further research.

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Section: Discussionmentioning

confidence: 99%

Synergism Antiproliferative Effects of Apigenin and Naringenin in NSCLC Cells

et al. 2023

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“…Dehidroepiandrosteron ile indüklenmiş polikistik over sendrom sıçan modelinde apigeninin lipit profilini ve antioksidan durumunu iyileştirerek koruyucu etki gösterdiği ve over fonksiyonunu restore ettiği rapor edilmiştir 33 . Yapılan başka bir çalışmadan elde edilen sonuçlarda ise apigeninin güçlü anti-oksidan, anti-inflamatuar ve anti-apoptotik etkileri nedeniyle kurşun maruziyetiyle ilişkili moleküler, biyokimyasal ve histolojik değişiklikleri azaltmak için kullanılabileceği gösterilmiştir 34 . Kim ve arkadaşlarının yaptığı bir araştırmada ise apigeninin antioksidan etki göstererek miyelin ve periferik aksonların bozulmasını önlediği ve periferik sinir dejenerasyonunu etkili bir şekilde geciktirdiği bildirilmiştir 35 .…”

Section: Apigenin'in Anti-oksidan Etkisiunclassified

Apigenin'in potansiyel farmakolojik etkileri üzerine bir derleme

SUSAM,

ÇIKIM

2023

aktd

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Apigenin, günlük hayatta tükettiğimiz meyve ve sebzelerde bolca bulunan, çeşitli sağlık sorunlarının önlenmesinde ve tedavisinde önemli bir rol oynayan flavonoidlerden biridir. Apigeninin, başlıca anti-oksidan, anti-inflamatuvar ve anti-neoplastik olmak üzere çeşitli farmokolojik etkileri bulunmakla birlikte, bu etkilerini spesifik yolaklardaki proteinleri up ya da down regüle ederek sergilemektedir. Bu çalışmada apigeninin özellikle inflamasyon, oksidan-antioksidan denge, kanser, apoptozis ve hücre döngüsü üzerine etkilerine odaklanılmış ve bu özellikleri in vivo ve in vitro çalışmalarla desteklenmiştir. Yapılan araştırmalar neticesinde apigeninin anti-inflamatuvar, anti-oksidan ve anti-kanserojen özellikler sergilediği neticesine varılmıştır. Bununla birlikte apigeninin hasar görmüş, yıpranmış ya da kanseröz hale dönüşmüş hücreleri apoptozise yönlendirdiği, hücre döngüsünü çeşitli kontrol noktalarında durdurarak bu tür hücrelerin çoğalmasını engellediği ve bu şekilde antiproliferatif etki sergilediği gözlenmiştir.

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Hepatoprotective Effect of Nicotinamide Versus Lead-Motivated Hepatotoxicity in Rats via Correcting Effect on Nuclear Factor-kβ Pathway and Glutathione Metabolism

Mahdavifard,

Shahi

2023

Biol Trace Elem Res

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Many years ago, until now, lead (Pb) poisoning is one of the pivotal environmental issues. Pb prompts liver dysfunction by elevating in ammation following oxidative stress. Consequently, we for the rst time investigated the effect of nicotinamide (B3) on the rat's liver histopathological and biochemical pro les in a rat model of Pb toxicity. Materials and MethodsThirty-six rats were shared into four groups (nine rats in each): untreated normal (N), B3 treated normal (N-B3), lead toxicity (Pbt), and B3 lead toxicity (Pbt-B3). Treated groups took B3 (180 mg/L in drinking water for one month). Pb intoxication was motivated in rats by acquiring 50 mg/l lead acetate from drinking water. Oxidative stress markers (advanced protein oxidation products, and malondialdehyde), antioxidant markers (total glutathione, reduced (GSH) to oxidized (GSSG) glutathione ratio, ferric ion reducing power, catalase, and paraoxonase-1), and in ammatory markers (hepatic nuclear factor-kβ expression, interleukin 1β level, and myeloperoxidase activity) in sera and liver homogenates were determined. Further, Biochemical liver function indicators (Alanine transaminase, aspartate transaminase, alkaline phosphatase, gamma-glutamyl transpeptidase, total bilirubin, total protein, albumin, and globulins) were quanti ed. Pb-induced liver damage was assessed with Histopathological observation.Results: B3 corrected lead-persuaded biochemical and histopathological changes in the rat's liver. In addition, treatment diminished Pb, oxidative stress, and in ammatory markers in the sera and liver homogenates of N-B3 and Pbt-B3 groups as well as elevated antioxidant markers (p < 0.001). ConclusionsNicotinamide through a decrease in Pb, oxidative stress, and in ammation prevented Pb prompted liver histopathological alternations and reduced liver dysfunction parameters.

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Apigenin protects from hepatorenal damage caused by lead acetate in rats

Cited by 5 publications

References 47 publications

Synergism Antiproliferative Effects of Apigenin and Naringenin in NSCLC Cells

Synergism Antiproliferative Effects of Apigenin and Naringenin in NSCLC Cells

Apigenin'in potansiyel farmakolojik etkileri üzerine bir derleme

Hepatoprotective Effect of Nicotinamide Versus Lead-Motivated Hepatotoxicity in Rats via Correcting Effect on Nuclear Factor-kβ Pathway and Glutathione Metabolism

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