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. 2017 Oct 2;22(10):1654.
doi: 10.3390/molecules22101654.

Protective Effects of Parkia biglobosa Protein Isolate on Streptozotocin-Induced Hepatic Damage and Oxidative Stress in Diabetic Male Rats

Affiliations

Protective Effects of Parkia biglobosa Protein Isolate on Streptozotocin-Induced Hepatic Damage and Oxidative Stress in Diabetic Male Rats

Bolajoko Idiat Ogunyinka et al. Molecules. .

Abstract

This study sought to investigate the possible protective role of Parkia biglobosa seed protein isolate (PBPi) against streptozotocin-induced hepatic damage and oxidative stress in diabetic male rats. Prior to animal experiments, a HPLC fingerprint of PBPi was recorded. Diabetes was induced in rats by a single intraperitoneal injection of streptozotocin (STZ; 60 mg/kg body weight). Diabetic rats were orally treated daily with PBPi (200 or 400 mg/kg body weight) or insulin (5 U/kg, i.p.) for 28 days. The degree of protection was evaluated using biochemical parameters such as malondialdehyde (MDA) levels, serum transaminases (ALT and AST), total protein, total glutathione (Total GSH), glutathione-S-transferase (GST), superoxide dismutase (SOD), catalase (CAT), and interleukin-6 (IL-6) activities. Histology of liver sections was also performed. The HPLC fingerprint of PBPi revealed eleven distinct peaks; PBPi at tested doses significantly attenuates STZ-induced elevated levels of serum IL-6, ALT and AST; and hepatic TBARS levels. Hepatic antioxidants (Total GSH, GST, SOD, CAT) as well as total protein were markedly restored in a dose-dependent manner. Histopathological results strongly support the protective role of PBPi. These results suggest PBPi could confer protection by ameliorating hepatic damage and oxidative stress caused by STZ in animal model possibly via its anti-inflammatory and antioxidant properties.

Keywords: HPLC; Parkia biglobosa; STZ-induced diabetes; hepatic antioxidant; histology; oxidative stress.

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Conflict of interest statement

The authors declare no conflict of interests.

Figures

Figure 1
Figure 1
HPLC fingerprint of Parkia biglobosa protein isolate.
Figure 2
Figure 2
Effect of PBPi on serum liver function and serum interleukin-6 (IL-6). (A) AST (U/L), (B) ALT (U/L), (C) Protein (mg/dL), (D) Interleukin-6 (pg/mL). Data are presented as mean ± S.D. (n = 10). Mean differences are significant (p < 0.05) when compared with: a control group, b STZ only.
Figure 3
Figure 3
Effect of PBPi on assessment of oxidative stress and antioxidants. (A) TBARS (nmol/mg protein), (B) Total GSH (μmol/mg protein), (C) GST (nmol/mg protein), (D) SOD (μ/mg protein), (E) CAT (nmol/mg protein). Data are presented as mean ± S.D. (n = 10). Mean differences are significant (p < 0.05) when compared with: a control group, b STZ only. Thiobarbituric acid reactive substances (TBARS), total reduced glutathione (Total GSH), glutathione-S-transferase (GST), superoxide dismutase (SOD), catalase (CAT).
Figure 4
Figure 4
Histological examination of rat livers stained with hematoxylin and eosin (H&E). (A) Control: showing liver tissue with normal architecture; (B) PI 200ND: showing liver tissue with normal architecture; (C) PI 400ND: showing liver tissue with normal architecture; (D) STZ: showing expanded portal tracts by a severe lymphocytic infiltrate associated with necrotic hepatocytes focally; (E) STZ I: showing liver tissue with a mild lymphocytic infiltrate present within the portal tracts (F) STZ PI 200: showing the presence of very mild lymphocytic infiltrate within the portal tracts and the lobules, with mild focal necro-inflammatory changes; (G) STZ PI 400: showing regenerative changes within the hepatocytes even though there are very mild necro-inflammatory foci. (Scale bar = 310 μm).

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