Abstract
Kaff-e-Maryam (
Anastatica hierochuntica
L.) is extensively used to treat a range of health problems, most notably to ease childbirth and alleviate reproductive system-related disorders. This study aimed to evaluate the effect of
A. hierochuntica
ethanolic (KEE), and aqueous (KAE) extracts on CCl
4
-induced oxidative stress and nephrotoxicity in rats using the biochemical markers for renal functions and antioxidant status as well as histopathological examinations of kidney tissue.
A. hierochuntica
contained 67.49 mg GAE g
−1
of total phenolic compounds (TPC), 3.51 µg g
−1
of total carotenoids (TC), and 49.78 and 17.45 mg QE g
−1
of total flavonoids (TF) and total flavonols (TFL), respectively. It resulted in 128.71 µmol of TE g
−1
of DPPH-RSA and 141.92 µmol of TE g
−1
of ABTS-RSA.
A. hierochuntica
presented superior antioxidant activity by inhibiting linoleic acid radicals and chelating oxidation metals. The HPLC analysis resulted in 9 and 21 phenolic acids and 6 and 2 flavonoids in KEE and KAE with a predominance of sinapic and syringic acids, respectively. Intramuscular injection of vit. E + Se and oral administration of KEE, KAE, and KEE + KAE at 250 mg kg
−1
body weight significantly restored serum creatinine, urea, K, total protein, and albumin levels. Additionally, they reduced malondialdehyde (MOD), restored reduced-glutathione (GSH), and enhanced superoxide dismutase (SOD) levels. KEE, KAE, and KEE + KAE protected the kidneys from CCl
4
-nephrotoxicity as they mainly attenuated induced oxidative stress. Total nephroprotection was about 83.27%, 97.62%, and 78.85% for KEE, KAE, and KEE + KAE, respectively. Both vit. E + Se and
A. hierochuntica
extracts attenuated the histopathological alteration in CCl
4
-treated rats. In conclusion,
A. hierochuntica
, especially KAE, has the potential capability to restore oxidative stability and improve kidney function after CCl
4
acute kidney injury better than KEE. Therefore,
A. hierochuntica
has the potential to be a useful therapeutic agent in the treatment of drug-induced nephrotoxicity.