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<p>Cyclophosphamide (CYP), a well-known synthetic antineoplastic drug, has limited usage because of its ability to induce oxidative stress, leading to liver and kidney tissue damage, and the need to prevent the associated toxicity is very crucial. Therefore, this study evaluated the protective effect of crude extract, hexane–acetone (hex-ace), and methanol (MeOH) fractions of SIS on some renal and hepatic indices of cyclophosphamide-induced toxicity in male rats. Forty-two albino rats were randomly assigned to seven groups and given different treatments: group 1, normal control; group 2, CYP (15 mg/kg b.w. twice weekly) treated rats; groups 3 through 7, co-treatment of CYP and 100 mg/kg b.w. of hexane extract of SIS (HESIS), co-treatment of CYP and 200 mg/kg b.w. of HESIS, co-treatment of CYP and 400 mg/kg b.w. of HESIS, co-treatment of CYP and 200 mg/kg b.w. of hexane–acetone fraction of SIS (HAFSIS), and co-treatment of CYP and 200 mg/kg b.w. of methanol fraction of SIS (MFSIS), respectively, for 28 days. The compounds of SIS identified by GCMS were docked for enhancement of the Nrf2 signaling pathway using Open Babel, Discovery Studio, and PyRX. Administration of CYP significantly induced oxidative stress-related renal and hepatic injury as seen in the CYP-treated group compared to the normal rats, but the SIS extract and fractions significantly (<i>P</i> &lt; 0.05) reduced the evaluated renal and hepatic indices and enhanced the SOD and CAT compared to the CYP-treated group. The SIS-identified bioactive compounds through an in silico study showed high potential in upregulating and enhancing the Nrf2 signaling pathway, which accounts for the antioxidative stress potential of SIS. The n-hexadecanoic acid from SIS exhibited a docking score of − 7.8, and the control (tocopherol) was − 8.2 toward the studied Nrf2 targets. The outcome of the study showed that SIS possesses renal and hepatic protective potential against CYP-induced oxidative reno-hepatic injury, and it could serve as an adjunct and a good source of treatment for CYP-induced renal and hepatic toxicity.</p>

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Sesamum indicum seed (SIS) extract and fractions attenuated cyclophosphamide-induced hepato-reno toxicity via modulation of biochemical indices and enhancement of Nrf2 signaling pathway: in vivo and in silico study

  • 期刊论文

  • 发表日期：

    2025年4月8日

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  • Jacinta Chigozie Ukpabi-Ugo,
  • Chioma Assumpta Anosike,
  • Obinna Ajah,
  • Anthony Chinedum Cemaluk Egbuonu,
  • Celestine Ugwu Obiora,
  • Chidinma Doris Umeakuana

摘要

Cyclophosphamide (CYP), a well-known synthetic antineoplastic drug, has limited usage because of its ability to induce oxidative stress, leading to liver and kidney tissue damage, and the need to prevent the associated toxicity is very crucial. Therefore, this study evaluated the protective effect of crude extract, hexane–acetone (hex-ace), and methanol (MeOH) fractions of SIS on some renal and hepatic indices of cyclophosphamide-induced toxicity in male rats. Forty-two albino rats were randomly assigned to seven groups and given different treatments: group 1, normal control; group 2, CYP (15 mg/kg b.w. twice weekly) treated rats; groups 3 through 7, co-treatment of CYP and 100 mg/kg b.w. of hexane extract of SIS (HESIS), co-treatment of CYP and 200 mg/kg b.w. of HESIS, co-treatment of CYP and 400 mg/kg b.w. of HESIS, co-treatment of CYP and 200 mg/kg b.w. of hexane–acetone fraction of SIS (HAFSIS), and co-treatment of CYP and 200 mg/kg b.w. of methanol fraction of SIS (MFSIS), respectively, for 28 days. The compounds of SIS identified by GCMS were docked for enhancement of the Nrf2 signaling pathway using Open Babel, Discovery Studio, and PyRX. Administration of CYP significantly induced oxidative stress-related renal and hepatic injury as seen in the CYP-treated group compared to the normal rats, but the SIS extract and fractions significantly (P < 0.05) reduced the evaluated renal and hepatic indices and enhanced the SOD and CAT compared to the CYP-treated group. The SIS-identified bioactive compounds through an in silico study showed high potential in upregulating and enhancing the Nrf2 signaling pathway, which accounts for the antioxidative stress potential of SIS. The n-hexadecanoic acid from SIS exhibited a docking score of − 7.8, and the control (tocopherol) was − 8.2 toward the studied Nrf2 targets. The outcome of the study showed that SIS possesses renal and hepatic protective potential against CYP-induced oxidative reno-hepatic injury, and it could serve as an adjunct and a good source of treatment for CYP-induced renal and hepatic toxicity.