Evaluation of oxidative stress markers in type-2 diabetic rat kidney with treated Δ9-THC

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EVALUATION OF OXIDATIVE STRESS MARKERS IN TYPE-2

DIABETIC RAT KIDNEY WITH TREATED Δ

9

_-THC

FEBS EMBO 30 AUGUST - 4 SEPTEMBER 2014 PARİS, FRANCE

ZEYNEP MINE COSKUNa_{, KAROLIN YANAR}b_{, SEVAL AYDIN}b_{, SEMA BOLKENT}c

a_{Department of Molecular Biology and Genetics, Faculty of Arts and Sciences, Istanbul Bilim University, Istanbul, Turkey} b_{Department of Medical Biochemistry, Faculty of Cerrahpasa Medicine, Istanbul University, Istanbul, Turkey}

c_{Department of Medical Biology, Faculty of Cerrahpasa Medicine, Istanbul University, Istanbul, Turkey}

INTRODUCTION

MATERIAL AND METHOD

RESULTS

REFERENCES

[1] Li F et al. Protective effect of salidroside from Rhodiolae Radix on diabetes-induced oxidative stress in mice. Molecules 2011; 16: 9912-9924. [2] Baburao Jain A and Anand Jain V. Vitamin E, its beneficial role in diabetes mellitus (DM) and its complications. J Clin Diagn Res 2012; 6: 1624-1628. [3] Stadler K. Oxidative stress in diabetes. Adv Exp Med Biol 2012; 771: 272-287. [4] Ávila Dde L et al. Vildagliptin ameliorates oxidative stress and pancreatic beta cell destruction in type 1 diabetic rats. Arch Med Res 2013; 44: 194-202. [5] Ozbet E. Induction of oxidative stress in kidney. Int J Nephrology 2012; 465897: 9. [6] Bermúdez-Siva FJ et al. Activation of cannabinoid CB1 receptors induces glucose intolerance in rats. Eur J Pharmacol 2006; 531: 282-284. [7] Romero-Zerbo SY et al. Overexpression of cannabinoid CB2 receptor in the brain induces hyperglycemia and a lean phenotype in adult mice. J Neuroendocrinol 2012; 4: 1106-1119.

The male Sprague-Dawley rats (8-10 weeks) were

arranged as Control, Δ9-THC, Diabetes, Diabetes + Δ9

-THC groups. The type-2 diabetic rats were treated with a single dose nicotinamide (85 mg/kg) 15 min before the

injection of streptozotocin (65 mg/kg). Δ9_{-THC was}

administered intraperitoneally at 3 mg/kg/day for 7 days.

On day 15 after the Δ9_{-THC injections, kidney tissues}

were removed. Protein carbonyl (PCO), lipid

hydroperoxide (LHP), malondialdehyde (MDA), Cu-Zn superoxide dismutase (Cu-Zn, SOD) and thiol fractions

including total thiol (T-SH), protein thiol (P-SH) and nonprotein thiol (NP-SH) parameters were measured.

Statistical analysis was performed using the SPSS version 21.0 program.

Oxidative stress plays a major role in the pathogenesis of diabetes mellitus. Impaired redox homeostasis can lead to the damage of macromolecules and insulin resistance. Thus, oxidative stress promotes the development of

complication of diabetes [1-4]. It is suggested that diabetes induce oxidative stress in kidney [5]. Δ9

-tetrahydrocannabinol (Δ9_{-THC) has been shown to interfere with both the function of insulin and its release. The}

activation of cannabinoid receptors stimulates insulin secretion to maintain glucose homeostasis [6-7]. The current

study, we aimed to evaluate effects of Δ9_{-THC on oxidative stress markers with respect to antioxidant status in kidney}

tissue of streptozotosin + nicotinamid induced type 2 diabetic rats.

A significant increase was observed in PCO, LHP and MDA parameters of diabetic rats as compared to

control rats. Moreover, PCO, LHP and MDA levels of kidney were significantly reduced in diabetes treated

with Δ9_{-THC compared to diabetic animals. The SOD}

activity and T-SH level were shown a significant

increase in diabetic rats treated with Δ9_{-THC as}

compared with diabetic group. On the other hand, P-SH and NP-P-SH levels were non-significantly higher in

the diabetes treated with Δ9_{-THC than in the diabetic}

rats.

CONCLUSION

According to the results, the renal tissue in type 2 diabetic animals is exposed to oxidative damage. This

oxidative damage may be relieved in type 2 diabetic rats treated with

Δ

9

-THC.

Groups PCO* (nmol/mg) LHP* (µmol/mg) MDA* (µmol/mg) SOD* (U/mg) TSH* (nmol/mg) NPSH* (nmol/mg) PSH* (nmol/mg) Control (n=7) 1.89±0.08 0.23±0.01 1.34±0.10 3.06±0.13 4.00±0.32 0.87±0.20 3.13±0.38 Δ9_{-THC (n=6)} 3.90±0.52a 0.30±0.01 1.46±0.14 3.11±0.19 3.43±0.19 0.62±0.13 2.80±0.16

Diabetes (n=7) 3.70±0.41b 0.45±0.04a,c 2.74±0.28a,c 3.90±0.21e 2.93±0.35 0.68±0.10 2.25±0.31

Diabetes + Δ9-THC (n=7) 2.02±0.14c,d 0.35±0.01e,f 1.82±0.08d 5.30±0.30a,g,h 4.80±0.59f 1.16±0.16 3.63±0.69

P_ANOVA P <0.001 P<0.001 P<0.001 P<0.001 P<0.05 P>0.05 P>0.05

*Mean ± Standart Error of Mean (SEM)

a_{P<0.001 versus control;}b_{P<0.01 versus control;}c_{P<0.01 versus}Δ9_-THC;d_{P<0.01 versus diabetes;} e_{P<0.05 versus control;} f_{P<0.05 versus diabetes;}g_P<0.001

versus Δ9_-THC;h_{P<0.001 versus diabetes}