[Herbal supplement usage in cardiac patients]. / Kardiyoloji hastalarinda bitkisel ürün kullanimi.

OBJECTIVE: Complementary and alternative medicine (CAM) has become more and more widespread around the world. CAM is a broad term that refers to all medical healthcare services, methods, and practices that are not part of standard medical care, as well as the accompanying theories and beliefs. The aim of the present study was to investigate the use of herbal medicinal products in cardiac patients, as well as the methods of administration of the products. METHODS: This descriptive cross-sectional study included 199 patients aged over 18 years who were hospitalized in the Defne Hospital department of cardiology and volunteered to participate in a 20-item survey between April 2016 and June 2016. RESULTS: The study results indicated that 28.6% (n=57) of patients were using herbal products and 71.6% (n=142) said they did not. Only 14.03% (n=8) of those who used herbal products said they used them in consultation with their physician; 85.9% (n=49) had used herbal medicine without consulting their doctor. Of the participants with hypertension, 35.7% of them reported using herbal medicinal products. Of these, 22.5% of them were consuming lemon, 17.5% pomegranate syrup, and 17.5% green tea. Of the participants with cardiovascular diseases, 23.5% of them stated that they were taking herbal products. Of these, 25% were consuming green tea, 25% ginger, and 18.8% sage. CONCLUSION: Herbal medicinal supplements were used by a large portion of the cardiac patients in this study. Furthermore, most of the patients stated that they were using these products without informing their physician, a practice that can have unwanted consequences.

Protective Effect of Ellagic Acid on Paraquat-induced Kidney Hazards in Rats.

INTRODUCTION: Paraquat is a commonly used highly toxic herbicide. Despite many studies on detoxification of paraquat, an efficient and safe antidote has not been introduced for toxic cases in human being. The aim of this study was to investigate the effect of ellagic acid (EA) on paraquat-induced kidney hazards in rats. MATERIALS AND METHODS: Sixty rats were randomly assigned as controls and 5 treatment groups (n = 10 each) receiving EA only, paraquat at doses of 15 mg/kg and 45 mg/kg, and paraquat at the same doses plus EA. Paraquat was intraperitoneally injected and the EA was orally given. Kidney tissues were stained with hematoxylin-eosin for histopathologic investigation. RESULTS: Pathologic scoring showed that paraquat at the higher dose was associated with higher scores than the in the controls, EA group, and the high-dose paraquat group with EA treatment (P < .001 for all comparisons).  It was noted that paraquat caused a serious damage in the kidney and the EA treatment significantly reduced the extent of the damage. CONCLUSIONS: This study showed the protective effects of EA against paraquat-induced nephrotoxicity histologically. Ellagic acid provided significant improvement in glomerular and tubular structure.

Protective Effects of Intralipid and Caffeic Acid Phenethyl Ester (CAPE) on Hepatotoxicity and Pancreatic Injury Caused by Dichlorvos in Rats.

The present study was aimed to the investigate the protective effects of caffeic acid phenethyl ester (CAPE) and intralipid (IL) on hepatotoxicity and pancreatic injury caused by acute dichlorvos (D) intoxication in rats. Forty-eight Wistar rats were randomly divided into seven groups each containing seven rats except control groups. The groups included control, D, CAPE, IL, D + CAPE, D + IL, and D + CAPE + IL. Total antioxidant status and total oxidative stress levels were measured by automated colorimetric assay. Tissues were evaluated using hematoxylin and eosin (H&E) staining. Tissues were analyzed with hematoxylin and eosin by using standard protocols. Also, Bcl-2, Bax and caspase-3 were evaluated by immunohistochemical method in liver tissue. Total oxidant status in control, CAPE, and IL groups were significantly lower, and total antioxidant status in the D + CAPE, D + IL, and D + IL + CAPE groups were significantly higher compared to the D group. CAPE and IL treatment decreased the apoptotic and mitotic cell count in liver tissue. Parenchymal necrosis caused by dichlorvos is observed in pancreas tissues of rats. Mild congestion and edema formation occurred in pancreas tissues following D + CAPE and D + IL therapies. These results indicate that CAPE and IL have the potential to decrease oxidative stress and hepatic and pancreatic injuries caused by acute dichlorvos intoxication. These drugs can be considered as a new method for supportive and protective therapy against pesticide intoxication.

Effect of clozapine on locomotor activity and anxiety-related behavior in the neonatal mice administered MK-801.

Atypical antipsychotics have been used to treat fear and anxiety disturbance that are highly common in schizophrenic patients. It is suggested that disruptions of N-methyl-d-aspartate (NMDA)-mediated transmission of glutamate may underlie the pathophysiology of schizophrenia. The present study was conducted to analyze the effectiveness of clozapine on the anxiety-related behavior and locomotor function of the adult brain, which had previously undergone NMDA receptor blockade during a developmental period. In order to block the NMDA receptor, male mice were administered 0.25 mg/kg of MK-801 on days 7 to 10 postnatal. In adulthood, they were administered intraperitoneally 0.5 mg/kg of clozapine and tested with open-field and elevated plus maze test, to assess their emotional behavior and locomotor activity. In the group receiving MK-801 in the early developmental period the elevated plus maze test revealed a reduction in the anxiety-related behavior (p<0.05), while the open-field test indicated a decrease in locomotor activity (p<0.01). Despite these reductions, clozapine could not reverse the NMDA receptor blockade. Also, as an atypical antipsychotic agent, clozapine could not reverse impairment in the locomotor activity and anxiety-related behavior, induced by administration of the MK-801 in neonatal period.

Protective effects of caffeic acid phenethyl ester on dose-dependent intoxication of rats with paraquat.

PURPOSE: Paraquat (PQ; 1,1'dimethyl-bipyridilium 4,4'-dichloride), which is used extensively throughout the world, is highly toxic to humans. We aimed to investigate the protective effects of different doses of caffeic acid phenethyl ester (CAPE) on PQ-intoxicated rats. MATERIALS AND METHODS: A total of 80 rats were divided into the following eight groups, comprising 10 rats in each group: group 1: control; group 2: administered with CAPE (10 µmol/kg); group 3: administered with 15 mg/kg PQ (PQ15 group); group 4: administered with 30 mg/kg PQ (PQ30 group); group 5: administered with 45 mg/kg PQ (PQ45 group); group 6: administered with 15 mg/kg PQ + CAPE; group 7: administered with 30 mg/kg PQ + CAPE and group 8: administered with 45 mg/kg PQ + CAPE. Both PQ and CAPE were injected intraperitoneally. Pancreatic tissue was examined with both haematoxylin and eosin and immunochemical staining. RESULTS: The ratio of the immunohistochemical staining area to the total pancreatic area of the ß cells revealed that statistically significant differences were observed only between the PQ and PQ + CAPE groups (p < 0.05). DISCUSSION: The evaluation of the data suggests that CAPE can be used to prevent acute effects of PQ intoxication.

Ameliorating effects of CAPE on oxidative damage caused by pneumoperitoneum in rat lung tissue.

We investigated the biochemical and histopathological effects of caffeic acid phenethyl ester (CAPE) against oxidative stress causing lung injury induced by pneumoperitoneum. Twenty-eight rats were selected at random and seven rats were assigned to each of the following groups. The control group (S) was subjected to a sham operation without pneumoperitoneum. The other groups were subjected to CO2 pneumoperitoneum 15 mmHg for 60 min. The laparoscopy group (L) had no additional drugs administered, the laparoscopy + alcohol (LA) group had 1 ml of 70% ethyl alcohol administered 1 h before the desufflation period, and the laparoscopy + CAPE (LC) group had CAPE administered at 10 µmol/kg 1 h before the desufflation period. The total oxidative status levels of lung and plasma were significantly increased in the LA group as compared with the LC and S group. When the LC group was compared with the L group, there was a decrease in the level of total oxidant status and increase in the levels of total antioxidant status and paraoxonase in lung tissue. The level of total antioxidative status in the S group was increased compared with the L group in lung tissue and bronchoalveolar lavage fluid. TNF-α and IL-6 were found significantly elevated in the L group compared with the LC and S groups in bronchoalveolar lavage fluid. There was a similar increase in plasma levels of IL-6. These results were supported by histopathological examination. CAPE was found to considerably reduce oxidative stress and inflammation induced by pneumoperitoneum.

Effects of intralipid and caffeic acid phenethyl ester on neurotoxicity, oxidative stress, and acetylcholinesterase activity in acute chlorpyriphos intoxication.

UNLABELLED: Chlorpyriphos is one of the most widely used organophosphate (OP) insecticide in agriculture with potential toxicity. Current post-exposure treatments consist of anti-cholinergic drugs and oxime compounds. We studied the effects of intralipid and caffeic acid phenethyl ester (CAPE) on chlorpyriphos toxicity to compose an alternative or supportive treatment for OP poisoning. METHODS: Forty-nine rats were randomly divided into seven groups. Chlorpyriphos was administered for toxicity. Intralipid (IL) and CAPE administered immediately after chlorpyriphos. Serum acetylcholinesterase (AChE) level, total oxidant status (TOS), total antioxidant response (TAR), and histologic examination of cerebellum and brain tissue with Hematoxylin-Eosin and immunohistochemical dyes were examined. RESULTS: Serum enzym levels showed that chlorpyriphos and CAPE inhibited AChE while IL alone had no effect, chlorpyriphos and CAPE intensifies the inhibition effect. Significant difference at AChE levels between the chlorpyriphos+IL and chlorpyriphos+CAPE verified that IL has a protective effect on AChE inhibition. TAR levels were significantly increased in all groups except chlorpyriphos group, TOS levels revealed that CAPE and IL decrease the amount of oxidative stress. Histologic examination revealed that neuronal degeneration was slightly decreased at chlorpyriphos+IL group, but CAPE had a significant effect on protection of neuronal degeneration. CONCLUSION: The results of this study gave us three key points. 1) AChE activity is important for diagnosis of OP intoxication but it has no value for determining the neuro-degeneration. 2) CAPE inhibits AChE activity and may increase the muscarinic-nicotinic hyperactivation. Therefore it should not be used for treatment of OP intoxication. 3) IL decreases the severity of neurodegeneration and symptoms of OP intoxication and it can be used as a supportive agent.

Comparison of the chronic effects of ribavirin and caffeic acid phenethyl ester (CAPE) on pancreatic damage and hepatotoxicity.

UNLABELLED: This study was aimed to comparison of the effects of the chronic use of the Ribavirin and caffeic acid phenethyl ester (CAPE) on the pancreatic damage and hepatotoxicity in rats. METHODS: The rats were given orally 30 mg/kg/day doses of Ribavirin for 30 days, and intraperitoneally 10 µmol/kg doses of CAPE. The 37 rats were divided into 4 groups: (I) Control (n=7), (II) Ribavirin (R) (n=10), (III) CAPE (n=10), and (IV) R+CAPE (n=10). RESULTS: Ribavirin and CAPE yielded similar results in terms of Serum, total antioxidant status (TAS), total oxidant status (TOS), amylase, lipase, and insulin compared to the control group. However, while Ribavirin provided similar results with the control group in terms of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) enzymes, the CAPE group had elevated AST and ALT levels compared to the control group. Histopathologic evaluations revealed that CAPE or Ribavirin had no degenerative effects on both the pancreas and liver tissues. In this way, the biochemical results were confirmed by the histopathologic results. CONCLUSION: It can be concluded that Ribavirin does not lead to any pancreatic damage and hepatotoxicity, and has more beneficial effects than CAPE on especially liver tissue.

Oral intralipid emulsion use: a novel therapeutic approach to pancreatic ß-cell injury caused by malathion toxicity in rats.

We aimed to investigate whether oral intralipid emulsion (OIE) reduces pancreatic ß-cell injury (PßCI) by chelating with malathion (M), or increases PßCI by increasing M absorption in the stomach. Fifty rats were randomly divided into six groups: control group (C); OIE administered group (L); M-treated group (M); OIE-administered group immediately after given M (M0L); OIE-administered group 6 hours after being given M (M6L) and OIE administered group 12 hours after being given M (M12L). M induced PßCI, hyperglycemia, temporary hyperinsulinemia and oxidative stress (OS). However, there was no significant difference in serum levels of glucose, insulin, total oxidants (TOS) and liver TOS between the M0L group and groups C and L. Also, insulin levels of M12L significantly increased, compared to the M6L group. Biochemical results, which were confirmed by histopathology, indicate that administering OIE after 6 hours and immediately after taking M may markedly prevent PßCI, hyperglycemia and OS. In addition, OIE's effectiveness decreased after 6 hours and was totally ineffective after 12 hours. We concluded that OIE may help to achieve a better prognosis and reduce mortality rate in cases presented to the emergency department, particularly within the first 6 hours, resulting from organophosphate pesticide poisoning by oral ingestion.

Caffeic acid phenethyl ester (CAPE) protects against acute urogenital injury following pneumoperitoneum in the rat.

PURPOSE: Our aim is to determine the biochemical and histologic changes induced in the kidneys, testis and prostate on possible ischemia and reperfusion (I/R) injury caused by pneumoperitoneum (PNP) in a rat model and to evaluate the ability of protective effects of caffeic acid phenethyl ester (CAPE). METHODS: Twenty-eight adult male Wistar albino rats were randomly divided to one of three treatment groups, with seven animals in each group. Sham, laparoscopy (L), and laparoscopy plus CAPE (L + C) group were subjected to 60 min of PNP with 15 mmHg one hour before the desufflation period. Total oxidant status (TOS) and total antioxidant status (TAS) levels were determined in kidney, testis, and prostate. Kidney and testis tissues were removed to obtain a histologic score. Also, Johnsen scoring system was used for testicular tissue analysis. RESULTS: L group had significantly higher TOS and lower TAS levels on kidney and testis compared to the other groups. In prostate biochemical analysis, there was not any difference between groups. No difference was found between groups according to kidney and testis tissues' histologic evaluation. In evaluation of Johnsen scoring, L group showed significant lower score compared to the other two groups. CONCLUSIONS: Increased intraabdominal pressure (IAP) had an oxidative effect on kidney and testis but not on prostate in rats. Moreover, it could affect the testicular Johnsen score. All these adverse effects of IAP on both kidney and testis could be prevented by CAPE administration.

Effects of sildenafil citrate, isoniazid, and streptomycin on testicular tissue and epididymal semen quality in rats.

OBJECTIVE: To evaluate the effects of isoniazid (INH) and streptomycin (STR) on epididymal semen quality and testicular tissue, and to evaluate the protective effect of sildenafil citrate (SC) on possible testicular toxicity induced by STR and INH in rats. METHODS: Eighty adult male Sprague-Dawley rats were divided randomly into 8 groups including control, SC, INH, STR, STR+INH, SC+INH, SC+STR, and SC+INH+STR. After 45 days of treatment, the reproductive organ weights, epididymal semen quality, testicular histopathological findings, levels of serum nitric oxide, testosterone, follicle-stimulating hormone (FSH) and luteinizing hormone (LH) were investigated. RESULTS: SC significantly increased the epididymal sperm motility and concentration, and the levels of FSH, LH, and testosterone. The STR group had a significantly higher percentage of sperm head defect than the control group (P < .05). The INH group had lower Johnsen Testicular Biopsy Score than the control group (P < .001). Although SC and INH treatment alone did not affect the epididymal semen quality negatively, the SC+INH group had significantly higher spermatozoon tail and total morphologic defect ratios than the control group (P < .05). CONCLUSION: It has been concluded from this study that (1) SC has positive effects on spermatogenesis, sperm production, and semen quality; (2) STR affected the testicular biopsy score and spermatozoon head morphology negatively, but positively affected the other spermatologic traits; (3) INH did not effect the epididymal semen quality negatively, but decreased testicular biopsy score; and (4) SC can prevent the spermatozoon head defects induced by STR and can decrease the testicular toxicity induced by INH.

The protective effects of curcumin on intestine and remote organs against mesenteric ischemia/reperfusion injury.

BACKGROUND/AIMS: Mesenteric ischemia/reperfusion injury induces a systemic response and releases harmful substances that may affect distant organs such as the lung, liver and kidney. We designed this study to determine if curcumin has protective effects against mesenteric ischemia/reperfusion injury and mesenteric ischemia/reperfusion-induced intestinal and distant organ injury. METHODS: Forty Wistar-Albino rats were divided into four groups as: sham, control, ischemia/reperfusion, and ischemia/reperfusion+curcumin. The ischemia/reperfusion and ischemia/reperfusion+curcumin groups were subjected to mesenteric arterial ischemia for 30 minutes and reperfusion for 1 hour. The control and ischemia/reperfusion+curcumin groups were administered curcumin (200 mg/kg, single dose) via oral gavage 15 min before the injury insult. Blood and pulmonary, hepatic and kidney tissue specimens were obtained to measure serum malondialdehyde and total antioxidant capacity, tissue levels of total antioxidant capacity, total oxidative status, and oxidative stress index. In addition, intestine, pulmonary, hepatic, and kidney tissue specimens were obtained for the evaluation of histopathological changes. RESULTS: The histopathological injury scores of the intestine and distant organs were significantly higher in the ischemia/reperfusion group; these injuries were prevented by curcumin in the ischemia/reperfusion+curcumin group. In the ischemia/reperfusion group, a significant increase in serum malondialdehyde levels was determined, which was prevented with curcumin pretreatment in the ischemia/reperfusion+curcumin group. Total antioxidant capacity levels were significantly supported by curcumin pretreatment in the control and ischemia/reperfusion+curcumin groups. CONCLUSIONS: This study demonstrated that curcumin ameliorates histopathological damage in the intestine and distant organs against mesenteric ischemia/reperfusion injury.

Protective effects of beta glucan and gliclazide on brain tissue and sciatic nerve of diabetic rats induced by streptozosin.

There have not been yet enough studies about effects of beta glucan and gliclazide on oxidative stress created by streptozotocin in the brain and sciatic nerve of diabetic rats. The aim of this paper was to investigate the antioxidant effects of gliclazide and beta glucan on oxidative stress and lipid peroxidation created by streptozotosin in brain and sciatic nerve. Total of 42 rats were divided into 6 groups including control, diabetic untreated (DM) (only STZ, diabetic), STZ (DM) + beta glucan, STZ (DM) + gliclazide, only beta glucan treated (no diabetic), and only gliclazide treated (no diabetic). The brain and sciatic nerve tissue samples were analyzed for malondialdehyde (MDA), total oxidant status (TOS), total antioxidant status (TAS), oxidative stress index (OSI), and paraoxonase (PON-1) levels. We found a significant increase in MDA, TOS, and OSI along with a reduction in TAS level, catalase, and PON-1 activities in brain and sciatic nerve of streptozotocin-induced diabetic rats. Also, this study shows that in terms of these parameters both gliclazide and beta glucan have a neuroprotective effect on the brain and sciatic nerve of the streptozotocin-induced diabetic rat. Our conclusion was that gliclazide and beta glucan have antioxidant effects on the brain and sciatic nerve of the streptozotocin-induced diabetic rat.

Oxidative damage is ameliorated by curcumin treatment in brain and sciatic nerve of diabetic rats.

To date, there have not been enough studies about the effects of curcumin against oxidative stress on sciatic nerves caused by streptozotocin (STZ) in diabetic rats. Therefore, this study was undertaken to determine whether curcumin, by virtue of its antioxidant properties, could affect the oxidant/antioxidant balance in the sciatic nerve and brain tissues of streptozotocin (STZ)-induced diabetic rats. A total of 28 rats were randomly divided into four groups of seven rats each: normal controls, only curcumin treated, diabetic controls, and diabetics treated with curcumin. Biomarkers-malondialdehyde (MDA), total oxidant status (TOS), total antioxidant status (TAS), oxidative stress index (OSI), and NO levels-for oxidative stress in the brain and sciatic nerve tissues of the rats were measured. We found a significant increase in MDA, NO, TOS, and OSI, along with a reduction in TAS levels in the brains and sciatic nerves of the STZ-induced diabetic rats (for both parameters p < 0.05). The MDA, TOS, OSI, and NO levels in these tissues were significantly reduced in the curcumin-treated diabetic group compared to the untreated diabetic group. In conclusion, the results of this study suggested that curcumin exhibits neuroprotective effects against oxidative damage in the brain and sciatic tissues of diabetic rats.

The anti-oxidant and anti-apoptotic effects of nebivolol and zofenopril in a model of cerebral ischemia/reperfusion in rats.

The aim of this experiment was to investigate whether nebivolol and zofenopril have protective effects against oxidative damage and apoptosis induced by cerebral ischemia/reperfusion (I/R). There were seven groups of rats, with each containing eight rats. The groups were: the control group, I/R group, I/R plus zofenopril, I/R plus nebivolol, I/R plus nebivolol and zofenopril, zofenopril only and nebivolol only. Cerebral I/R was induced by clamping the bilateral common carotid artery and through hypotension. The rats were sacrificed 1h after ischemia, and histopathological and biochemical analyses were carried out on their brains. The total antioxidant capacity was evaluated by using an automated and colorimetric measurement method developed by Erel. I/R produced a significant increase in the levels of total oxidant status and malondialdehyde levels, the number of caspase-3 immunopositive cells and activities of prolidase and paraoxonase in brain when compared with the control group (p<0.05). A significant decrease in brain total antioxidant capacity and nitric oxide levels were found in I/R group when compared with the control group (p<0.05). Both nebivolol and zofenopril treatment prevented decreasing of the total antioxidant capacity and nitric oxide levels, produced by I/R in the brain (p<0.05). Both nebivolol and zofenopril treatment prevented the total oxidant status, malondialdehyde levels, activities of paraoxonase and prolidase from increasing in brains of rats exposed to I/R (p<0.05). In conclusion, both nebivolol and zofenopril protected rats from ischemia-induced brain injury. The protection may be due to the indirect prevention of oxidative stress and apoptosis.

Ellagic acid attenuates oxidative stress on brain and sciatic nerve and improves histopathology of brain in streptozotocin-induced diabetic rats.

The aim of this study was to investigate the possible effects of ellagic acid in brain and sciatic nerve tissues of diabetic rats. Also, the impact of ellagic acid on catalase and paraoxonase (PON-1) activities, total antioxidant status (TAS), total oxidant status (TOS), oxidative stress index (OSI), malondialdehyde (MDA) and nitric oxide (NO) were examined. The rats were randomly divided into four groups, with eight rats each: Normal controls (not diabetic), only ellagic acid treated (ellagic acid controls, not diabetic), Diabetic controls (streptozotocin, diabetic), ellagic acid-treated diabetic (streptozotocin + ellagic acid). After a 4 week experiment, rats were sacrificed, and biomarkers for oxidative stress in the brain and sciatic nerve tissues of the rats were measured. There was significant depletion in the PON-1, catalase, and TAS levels in the brain and sciatic nerve tissues compared to the control groups (for both parameters, p<0.05). The values of catalase, PON-1 and TAS reversed back to normal levels in ellagic acid-treated diabetic rats compared to untreated diabetic rats (for both parameters, p<0.05). The levels of MDA, TOS, NO and, OSI in the brain and sciatic nerve tissues were higher in untreated diabetic rats compared to control group (for both parameters p<0.05). However, MDA, TOS, OSI, and NO levels were found to be significantly reduced in the ellagic acid-treated diabetic group compared to the untreated diabetic group in these tissues (for both parameters, p<0.05). In conclusion, the results of the present study suggested that ellagic acid exhibits neuroprotective effects against oxidative damage in diabetic rats.

Ellagic acid ameliorates lung injury after intestinal ischemia-reperfusion.

BACKGROUND: The aim of this study was to investigate the possible protective role of antioxidant treatment with ellagic acid (EA) on lung injury after intestinal ischemia-reperfusion (I/R) injury using biochemical and histopatological approaches. MATERIALS AND METHODS: Forty rats were divided into four groups as control, control + EA, I/R, and I/R + EA. The control and control + EA groups were also anesthetized and subjected to laparotomy, but without clamp application. The control + EA and I/R + EA groups were given EA (85 mg/kg) orally prior to experiment. The I/R and I/R + EA groups underwent 30 minutes of intestinal ischemia and 1 hour of reperfusion. In all groups, serum total antioxidant capacity (TAC) and malondialdehyde (MDA) levels were determined. TAC, total oxidative status (TOS), and oxidative stress index (OSI) in lung tissue were measured. Lung tissue histopathology was also evaluated by light microscopy. RESULTS: TAC levels were higher in control, EA, and I/R + EA groups while TOS, OSI, and MDA levels were lower in these groups compared with I/R group. Serum MDA levels were significantly higher in I/R + EA group than that of control group. Lung tissue TAC levels were lower in I/R + EA group while OSI values were higher in that groups compared with EA group. Histological tissue damage was milder in the EA treatment group than in the I/R group. CONCLUSION: These results suggest that EA treatment protected the rats lung tissue against intestinal I/R injury.

Effects of exercise and caffeic acid phenethyl ester after chronic exercise rat model.

In order to understand whether exercise and caffeic acid phenethyl ester (CAPE) has an effect on obesity and weight control, we investigated the effects of CAPE, and exercise on lipid parameters (triglyceride, total cholesterol, HDL-C, LDL-C), and adipokine substances such as leptin and resistin in rats. 40 male rat were randomly assigned into 4 groups. It was determined that CAPE does not have any significant effect on these parameters but that lipid parameters and leptin values in exercise groups decreased considerably, while no significant change occurred in resistin levels. In order to understand whether diet has an effect on exercise, body weights of all animal groups in pre and post-exercise were compared. A significant weight gain was observed (p = 0.005) in all groups. This study concluded that exercise has a considerable effect on leptin and lipid parameters; however, exercise alone was not sufficient for weight control and could be effective in weight control only when accompanied by a restricted diet. Key pointsCaffeic acid phenethyl ester is not effective on weight control, lipid parameters, and adipokine substances such as leptin and resistin.Exercise can be effective in weight control only when accompanied by a restricted diet.