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<p>Acetaminophen (APAP) is a widely used analgesic and antipyretic, but its toxicity can lead to liver injury or failure. This study evaluated the hepatoprotective mechanisms of <i>L. speciosa</i> ethanolic leaf extract (LSE) against APAP-induced hepatic damage. Rats were randomly divided into five groups: Control (Cont), APAP (2&#xa0;g/kg b.w. single oral dose on day 22), LSE (500&#xa0;mg/kg b.w./day), APAP + LSE, and APAP + NAC (initial NAC dose of 100&#xa0;mg/kg b.w. two hours post-APAP, followed by maintenance doses every 12&#xa0;h). APAP-intoxicated rats showed leukocytosis, decreased erythrocyte count, Hb, and PCV, increased serum bilirubin, and elevated ALT, AST, and ALP activities. APAP intoxication also decreased plasma protein levels, albumin, and globulin while increasing liver MDA and depleting GSH. The expressions of hepatic SOD and CAT were reduced, while NF-κB, TNF-α, iNOS, Nrf2, and HO-1 were significantly upregulated. Also, APAP increased Bax and decreased Bcl-2. LSE improved most parameters, suppressing oxidative stress, inflammation, and apoptosis and regulating NF-κB, TNF-α, iNOS, Nrf2, HO-1, Bax, and Bcl-2 expression. Nevertheless, the deeper upstream molecular targets of LSE require further exploration. Its effects were comparable to NAC, with NAC showing slightly superior outcomes in some markers. Our findings suggest that LSE contains hepatoprotective phytochemicals capable of mitigating oxidative damage, inflammation, and apoptosis induced by APAP, supporting its potential as a natural alternative for managing drug-induced liver injury.</p>

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Lagerstroemia Speciosa (L.) Pers mitigates acetaminophen-induced acute liver toxicity in rats through modulations of oxidative stress, inflammation, apoptosis and the NF-κB/TNF-α/iNOS, Nrf2/HO-1, signaling pathways

  • 期刊论文

  • 发表日期：

    2025年7月23日

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  • Nagham E. Elsheshtawy,
  • Fatma M. Abdelhamid,
  • Engy F. Risha,
  • Hebatallah A. Mahgoub,
  • Ahmed I. Ateya,
  • Mohamed E. El-Boshy

摘要

Acetaminophen (APAP) is a widely used analgesic and antipyretic, but its toxicity can lead to liver injury or failure. This study evaluated the hepatoprotective mechanisms of L. speciosa ethanolic leaf extract (LSE) against APAP-induced hepatic damage. Rats were randomly divided into five groups: Control (Cont), APAP (2 g/kg b.w. single oral dose on day 22), LSE (500 mg/kg b.w./day), APAP + LSE, and APAP + NAC (initial NAC dose of 100 mg/kg b.w. two hours post-APAP, followed by maintenance doses every 12 h). APAP-intoxicated rats showed leukocytosis, decreased erythrocyte count, Hb, and PCV, increased serum bilirubin, and elevated ALT, AST, and ALP activities. APAP intoxication also decreased plasma protein levels, albumin, and globulin while increasing liver MDA and depleting GSH. The expressions of hepatic SOD and CAT were reduced, while NF-κB, TNF-α, iNOS, Nrf2, and HO-1 were significantly upregulated. Also, APAP increased Bax and decreased Bcl-2. LSE improved most parameters, suppressing oxidative stress, inflammation, and apoptosis and regulating NF-κB, TNF-α, iNOS, Nrf2, HO-1, Bax, and Bcl-2 expression. Nevertheless, the deeper upstream molecular targets of LSE require further exploration. Its effects were comparable to NAC, with NAC showing slightly superior outcomes in some markers. Our findings suggest that LSE contains hepatoprotective phytochemicals capable of mitigating oxidative damage, inflammation, and apoptosis induced by APAP, supporting its potential as a natural alternative for managing drug-induced liver injury.