الفهرس 
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Abstract
The global efforts have been banded together for finding and synthesizing new drugs with higher potentiality and lesser side effects aiming to decrease the compications of diabetes.
Growing evidence has linked a low-grade chronic inflammatory response to diabetic mellitus and its complications.
Studies have showen a deeper conclusion of the function of inflammation and its interaction with other factors in the pathogenesis of type 2 diabetes. Activation of the inflammatory response and increasing expression of proinflammatory cytokines.
This finding should motivate scientists and researchers to develop an approach that can supress inflammation to control of diabetes mellitus.
In recent years, scientists have turned to various flavonoids to explain some of the health benefits associated with diets rich in fruits and vegetables, flavonoids are powerful antioxidants with anti-inflammatory and immune system benefits. Diets rich in flavonoid-containing foods are sometimes associated with cancer, neurodegenerative and cardiovascular disease prevention, moreover, it has role in skin protection, brain function, blood sugar and blood pressure regulation, in addition to antioxidant and anti-inflammatory activity.
Morin is a member of flavonoids, which found in many herbs such as red wine, and fruits like guava, chestnut, sweet, onion and almond, it has been demonstrated to own antioxidant, anti-inflammatory, antihypertensive, neuroprotective, and anticancer activity.
It is reported that morin able to demonstrate various biological activities involving antidiabetic, antioxidant, anti-inflammatory, cytoprotection, anticarcinogenic effects and antimutagenesis.
The present study was designed to evaluate the anti-inflammatory effect of morin against cardiac inflammation in diabetic rats through the control of the antioxidant status, its anti-inflammatory effect and efficacy against fibrosis in hearts of streptozotocin (STZ) - induced diabetic rats.
The work comprises a series of in vivo investigations, and to achieve the goal of the study, fourty male Wister rats were used and allocated into 4 groups, ten rats for each group as following:
group 1 (Control): Control (C): Normal healthy rats orally administered regular diet vehicle (0.5% sodium carboxymethyl cellulose solution).
group 2 (DM): STZ-treated rats were fed with HFD (58% fat, 25% protein and 17% carbohydrate, as a percentage of total kcal) (Reed et al., 2000) for 12 weeks and given a single dose of streptozotocin (i.p.) at 30 mg/kg following a 12 h fast at the seventh week to induce hyperglycemia and hypercholesterolemia. This group was also called HSFD/streptozotocin group.
group 3 (Morin): Normal healthy rats orally administered morin (30 mg/Kg body weight/day, daily for consecutive 6 weeks via gavages according to (Franova et al., 2016).
group (DM + morin): rats were treated as the third group STZ-treated rats orally administered except that they were orally administered morin (30 mg/kg/day) daily for consecutive 6 weeks, 72 h after streptozotocin (STZ) injection.
The animals were sacrificed 24 hours after receiving the last dose of distilled water after a fasting period of 12 hours. Rats were anaesthetized with light ether, pancreas and heart tissues were rapidly excised and blood samples obtained via heart puncture by sterilized syringe for assessment of metabolic disorder and biochemical markers; Fasting blood sugar (FBS), Hemoglobin A1c (HbA1c), total cholesterol, triglyceride, low density lipoprotein (LDL) and high-density lipoprotein (HDL). Aspartate Aminotransferase (AST), creatinine kinase (CK) and lactate dehydrogenase (LDH) as mrkers for cardiac damage are estimated in the plasma of rats. Superoxide dismutase (SOD) as a free radical scavengers of the antioxidant defense system estimated and malonaldyhide (MDA) in the heart homogenate is measured as well. Proinflammatory cytokines, interleukin-6 (IL-6) and tumor necrosis factor (TNF-α) are estimated in heart homgenate. Signaling growth factors and fibrogenic factors are estimated in heart homogenate such as glucose transporter type 4 (GLUT-4), transforming growth factor beta (TGF- β1), signal transducer and activator of transcription 3 (STAT3), janus kinase 2 (JAK-2), mitogen-activated protein kinases (MAPK), extracellular signal-regulated kinases (ERK). This work also included histopathological studies for all groups as well.
The results of the present study can be summarized as follows:
1. The biochemical studies revealed that HFD rats injected with the STZ showed marked increase in F.B.S, HBA1C, cholesterol, tri-glycerid, HDL- cholesterol and a marked increase in LDL- cholesterol. There was also a marked increase in AST, CK and LDH in addition a marked decrease in heart homogenate antioxidant enzyme SOD on the other hand there was a marked increase in MDA. There was also a marked increase in pro-inflammtory cytokined IL-6 and TNF- α. Moreover, there was a significant decrease in GLUT-4 however there was significant increase in TGF-β, STAT3, JAK-2, MAPK and ERK heart homogenate.
2. The histopathological investigations of myocardial tissues of HFD rats injected with the STZ revealed that swelling of cardiac muscle fibers with focal areas of coagulative necrosis which appeared as deeply eosinophilic areas (++). Massive mononuclealar cells infiltration mainly lymphocytes and macrophages especially around coronary blood vessels (+++) and oedema in-between muscle fibers (++) were noticed.
3. Treatment of HFD/ STZ rats with morin revealed a marked decrease in F.B.S, HBA1C, cholesterol, tri-glycerid, LDL- cholesterol and a marked increase in HDL- cholesterol. There was also a marked decrease in AST, CK and LDH in addition a marked increase in heart homogenate antioxidant enzyme SOD on the other hand there was a marked decrease in MDA. There was also a marked decrease in pro-inflammtory cytokined IL-6 and TNF- α. Moreover, there was a significant increase in GLUT-4 however there was significant decrease in TGF-β, STAT3, JAK-2, MAPK and ERK heart homogenate.
4. The histopathological investigations of HFD/ STZ rats which treated with morin showed the same histological picture of untreated group. Pancreatic acinar epithelial lining revealed vacuolation and necrosis. Shrinkage and loss of Langerhan’s Islet, on the other side, myocardial muscle showed improvement in comparison with diabetic induced group. Cardiac muscle appeared normal with less necrosis (-), edema (+) and inflammation (+).
In conclusion, the aforementioned results revealed that morin posses the ability to imoprove the cardiac inflammation associated with type 2 diabetic pateints.