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downregulation of angiogenic and proliferative markers i.e. VEGF, Hif1α and heat shock

protein 90 thus, indicating the antiangiogenic and antiproliferative activity of these
compounds.

5. PROTECTIVE EFFECTS OF NARINGENIN AGAINST METAL INDUCED
TOXICITY

Several authors have investigated the protective efficacy of NG against Cd induced
toxicity in tissues of various animal models. For instance, Renugadevi and Prabu (2009)

investigated the mitigatory effects of NG on Cd-induced nephrotoxicity in rats. Rats orally

administrated with cadmium chloride (5 mg/(kg day) for 4 weeks significantly induced the
renal damage as evident from the increased levels of serum urea, uric acid, creatinine; also

significantly decreased the levels of urea, uric acid and creatinine in urine. A noticeable

increase in the level of LPO and decrease in SOD, CAT, GPx and GST were also observed in
Cd-treated rats. Co-administration of NG (25 and 50 mg/kg day) along with Cd resulted in a

reversal of Cd-induced biochemical changes in kidney accompanied by a significant decrease
in LPO and an increase in the level of renal antioxidant defense system. The

histopathological studies in the kidney of rats also showed that NG (50 mg/kg day) markedly
reduced the toxicity of Cd and preserved the normal histological architecture of the renal

tissue.

The administration of NG at a dose of 25 or 50 mg/kg b.w. partially prevented an

increase in the activities of ALT, AST, LDH and GGT in the serum, and in the concentration
of bilirubin caused by co‐treatment with CdCl2. NG at a dose of 50 mg/kg b.w., significantly

attenuated a Cd‐induced decrease in the activities of enzymatic antioxidants (e.g., SOD,
CAT, GPx, GR and GST), as well as glucose 6‐phosphate dehydrogenase in liver. They also

observed NG administration provided partial protection from a decrease in the concentrations
of non‐enzymatic antioxidants (e.g., GSH, vitamin C and vitamin E), significant decrease in

lipid peroxidation and oxidative protein damage induced by Cd in the liver. They also

demonstrated that NG consumption under prevented Cd-induced severe histological changes
in liver, such as fatty degeneration, inflammatory cells infiltration, vacuolization and necrosis

of hepatocytes (Renugadevi and Prabu, 2010). Similarly, the therapeutic effects of NG
against Cd induced oxidative hepatotoxicity in Wistar rats was also reported by Prabhu et al.

(2011).
The protective potential of the NG against Cd induced toxicity was evaluated

experimentally in Swiss albino mice by Das et al. (2016). They administered 4 and 8 mg/kg

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