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ஜர்னல் ஆஃப் மாலிகுலர் பயோமார்க்ஸ் & நோயறிதல்

ஐ.எஸ்.எஸ்.என்: 2155-9929

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PUFAs from Stem Bark of Alstonia boonei Synergistically Modulates Diabetic, Hepatic and Androgenic Damage by Low Expression of COX-2 and iNOS in Rats

Abstract

Ajiboye JA, Akintunde JK, Okewuyi SO and Okafor UE

PUFAs, from the stem bark extract of Alstonia boonei (SBEAB) was hypothesized to possess anti-inflammatory, antioxidant, anti-diabetic, pro-spermatogenic and hepatoprotective activities. The present study investigated the possible biochemical and molecular mechanisms underlying the hepatoprotective and testoprotective effects of SBEAB in diabetic rat. Biomarkers of hepatic and testicular damage, histological and immunohistochemical techniques were used. The expression of cyclooxygenase (COX-2) and inducible nitric oxide synthase (iNOS) were also estimated. SBEAB administered orally at dose of 100 mg/kg for 14 days significantly lowered the activities of serum transaminases and MDA levels induced by single intraperitoneal administration of streptozotoxin (STREP) (80 mg/kg) and preserved the integrity of both hepatocytes and spermatocytes. Also, SBEAB elevated the STREPinduced reduced activities of Δ5-17β-HSD and Δ5-17β-HSD with corresponding decrease in the activity of CAT. SBEAB inhibited the STREP induced expression of COX-2 and iNOS. The protective effect of SBEAB was compared to that of metaglomide (METAG), an established anti-diabetic drug. METAG treatment on hepatic damage was most efficacious in diabetic rats; followed by post and pre-treatment respectively while pre-and post-treatment were more efficacious on testicular damage than anti-diabetic drug. Furthermore, pre and post-treatment were more efficacious in preventing pro-inflammation and testicular cancer in diabetic rats than METAG-administration. We therefore concluded that the repression of genes encoding COX-2 and iNOS proteins by SBEAB validates the molecular basis of testicular protection and further suggests the links between the hepatocellular damage and male reproductive dysfunctions in diabetic individuals.

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