Alterations in copper homeostasis and oxidative stress biomarkers in women using the intrauterine device TCu380A

Copper ions participate in the Häber–Weiss reaction to produce ROS, which can be toxic when in excess. The purpose of this study was to measure the copper concentration (Cu) in the plasma of women using Cu-IUDs and determine (i) the effect of Cu on oxidative stress biomarkers, (ii) the levels of copper transport proteins in the plasma and (iii) the status of some liver damage markers in relation to the length of the intrauterine device use. Thirty-nine controls and 35 T380-IUD users were recruited. Various oxidative stress biomarkers, ceruloplasmin (CRP), metallothioneins (MTs), Cu and enzyme activities involved in liver function were measured in the plasma. The Cu concentration was higher in women with IUDs, concomitantly with time-dependent increases in the main oxidative stress biomarkers (TBARS, protein carbonyls, glutathione and nitrates + nitrites), hepatic enzymes (LDH and transaminases), MTs and CRP. We concluded that the use of Cu-IUDs for more than 2 consecutive years should be avoided in order to prevent oxidative damage.     

Protective effect of lipoic acid against methotrexate-induced oxidative stress in liver mitochondria

Methotrexate (MTX) is a folic acid antagonist widely used as a cytotoxic chemotherapeutic agent for leukemia and other malignancies. The purpose of this study was to investigate the damage caused by MTX on liver mitochondria and its protection by using antioxidant properties of lipoic acid. MTX substantially affects mitochondrial function by reducing glutathione levels leading to disturbances in antioxidant enzyme defense system. Lipoic acid occurs naturally in mitochondria as a coenzyme. In various studies lipoic acid has been convincingly shown to exhibit an antioxidant role when supplemented exogenously. We studied the effect of lipoic acid pre-treatment on the toxicity of MTX in mouse liver mitochondria focusing specifically on the oxidative stress. MTX caused a significant rise in the mitochondrial lipid peroxidation (LPO), protein carbonyl (PC) content and superoxide radical generation. It also affected the mitochondrial thiol profile. Pre-treatment of mice with lipoic acid (35 mg/kg) markedly lowered mitochondrial LPO, PC content and superoxide radical generation. It also restored decreased enzymatic and non-enzymatic antioxidants of mitochondria. It is suggested that lipoic acid has a potential role in suppressing MTX-induced mitochondrial toxicity, and it affords protection either by reversing the decline of antioxidants or by the directly scavenging the free radicals.     

Locomotor damage and brain oxidative stress induced by lead exposure are attenuated by gallic acid treatment

We investigated the antioxidant potential of gallic acid (GA), a natural compound found in vegetal sources, on the motor and oxidative damages induced by lead. Rats exposed to lead (50 mg/kg, i.p., once a day, 5 days) were treated with GA (13.5 mg/kg, p.o.) or EDTA (110 mg/kg, i.p.) daily, for 3 days. Lead exposure decreased the locomotor and exploratory activities, reduced blood ALA-D activity, and increased brain catalase (CAT) activity without altering other antioxidant defenses. Brain oxidative stress (OS) estimated by lipid peroxidation (TBARS) and protein carbonyl were increased by lead. GA reversed the motor behavior parameters, the ALA-D activity, as well as the markers of OS changed by lead exposure. CAT activity remained high, possibly as a compensatory mechanism to eliminate hydroperoxides during lead poisoning. EDTA, a conventional chelating agent, was not beneficial on the lead-induced motor behavior and oxidative damages. Both GA (less) and EDTA (more) reduced the lead accumulation in brain tissue. Negative correlations were observed between the behavioral parameters and lipid peroxidation and the lead levels in brain tissue. In conclusion, GA may be an adjuvant in lead exposure, mainly by its antioxidant properties against the motor and oxidative damages resulting from such poisoning.     

Effect of taurine supplementation on cytochrome P450 2E1 and oxidative stress in the liver and kidneys of rats with streptozotocin-induced diabetes

To investigate whether diabetes-induced alterations of CYP2E1 and oxidative stress can be modulated by dietary taurine supplementation, male Wistar rats were divided into non-diabetic, diabetic, and diabetic taurine-supplemented groups (administered at 2% in the drinking water). Increased levels of CYP2E1-catalyzed p-nitrophenol hydroxylation were found in liver and kidney microsomes of rats with STZ-induced diabetes compared to those of non-diabetic control rats. Immunoblot and RT-PCR analyses of CYP2E1 protein and mRNA levels in the liver and kidneys showed the same trend as with enzyme activities. Taurine supplementation significantly decreased the enzyme activity and expression (protein and mRNA) of CYP2E1 in diabetic rat kidneys. Plasma β-hydroxybutyrate concentration was significantly reduced in taurine-treated diabetic rats. The induction of heme oxygenase-1 mRNA was suppressed by taurine treatment in diabetic rat kidneys. An increase in reduced glutathione (GSH) and a higher ratio of reduced to oxidized glutathione (GSH/GSSG) together with lower values of thiobarbituric acid-reactive substances (TBARS) were observed in the kidneys of taurine-treated diabetic rats. However, taurine supplementation caused only a slight or insignificant effect on these alternations in the liver of diabetic rats. Our results show dietary taurine may reduce CYP2E1 expression and activity, and oxidative stress in kidneys of diabetic rats.     

Ameliorating effect of curcumin on sodium arsenite-induced oxidative damage and lipid peroxidation in different rat organs

The present study was conducted to investigate the antioxidative effect of curcumin against sodium arsenite-induced oxidative damage in rat. Animals were divided into four groups, the first group was used as control. Groups 2, 3 and 4 were orally treated with curcumin (15 mg/kg BW), sodium arsenite (Sa, 5 mg/kg BW) and sodium arsenite plus curcumin, respectively. Rats were orally administered their respective doses daily for 30 days. Results showed that Sa increased thiobarbituric acid-reactive substances (TBARS) in plasma, liver, kidney, lung, testes and brain. While, the activities of glutathione S-transferase, superoxide dismutase and catalase and the content of sulfhydryl groups (SH-groups) were significantly decreased in plasma and tissues compared to control. Treatment with curcumin alone reduced the levels of TBARS, while induced the activities of the antioxidant enzymes, and the levels of SH-groups. The presence of curcumin with Sa reduced the induction in the levels of TBARS and induced the decrease in the activities of antioxidant enzymes and the levels of SH-groups. Results indicated that treatment with Sa decreased body weight and increased liver weight compared to control. The presence of curcumin with Sa alleviated its toxic effects. It can be concluded that curcumin has beneficial influences and could be able to antagonize Sa toxicity.     

Protective effect of grape seed proanthocyanidin extract against oxidative stress induced by cisplatin in rats

Cisplatin is one of the most potent chemotherapeutic antitumor drugs. Oxidative stress has been proven to be involved in cisplatin-induced toxicity. Therefore, the present study was undertaken to examine the antioxidant potential of grape seed proanthocyanidin extract (GSPE) against the toxicity of cisplatin in male rats. Cisplatin treated animals revealed a significant elevation in plasma, heart, kidney and liver thiobarbituric acid reactive substances (TBARS), while the activities of antioxidant enzymes (GST, SOD, CAT and GSH-Px, and the levels of glutathione (GSH) were decreased. Aspartate and alanine transaminases (AST and ALT), creatine kinase and lactate dehydrogenase were significantly increased in plasma, while liver AST and ALT were significantly decreased. Cisplatin significantly increased the levels of plasma total lipid, cholesterol, urea and creatinine, and the relative weight of kidney. On the other hand, plasma total protein and albumin, and body weight were significantly decreased. GSPE reduced cisplatin-induced the levels of TBARS in plasma, heart, kidney and liver, TL, cholesterol, urea and creatinine, and liver AST and ALT. Moreover, it ameliorated cisplatin-induced decrease in the activities of antioxidant enzymes, and GSH, total protein and albumin. Therefore, the present results revealed that GSPE exerts a protective effect by antagonizing cisplatin toxicity.     

Streptozotocin induced activation of oxidative stress responsive splenic cell signaling pathways: Protective role of arjunolic acid

Present study investigates the beneficial role of arjunolic acid (AA) against the alteration in the cytokine levels and simultaneous activation of oxidative stress responsive signaling pathways in spleen under hyperglycemic condition. Diabetes was induced by injection of streptozotocin (STZ) (at a dose of 70 mg/kg body weight, injected in the tail vain). STZ administration elevated the levels of IL-2 as well as IFN-γ and attenuated the level of TNF-α in the sera of diabetic animals. In addition, hyperglycemia is also associated with the increased production of intracellular reactive intermediates resulting with the elevation in lipid peroxidation, protein carbonylation and reduction in intracellular antioxidant defense. Investigating the oxidative stress responsive cell signaling pathways, increased expressions (immunoreactive concentrations) of phosphorylated p65 as well as its inhibitor protein phospho IκBα and phosphorylated mitogen activated protein kinases (MAPKs) have been observed in diabetic spleen tissue. Studies on isolated splenocytes revealed that hyperglycemia caused disruption of mitochondrial membrane potential, elevation in the concentration of cytosolic cytochrome c as well as activation of caspase 3 leading to apoptotic cell death. Histological examination revealed that diabetic induction depleted the white pulp scoring which is in agreement with the reduced immunological response. Treatment with AA prevented the hyperglycemia and its associated pathogenesis in spleen tissue. Results suggest that AA might act as an anti-diabetic and immunomodulatory agent against hyperglycemia.     

Effect of 3-butyl-1-phenyl-2-(phenyltelluro)oct-en-1-one on oxidative stress in cerebral cortex of rats

The objective of this study was to verify the effect of the organochalcogen 3-butyl-1-phenyl-2-(phenyltelluro)oct-en-1-one on some parameters of oxidative stress in the brain of 10-day-old rats. Cerebral cortex was incubated for 1 h in the presence or absence of 1, 10 or 30 μM of 3-butyl-1-phenyl-2-(phenyltelluro)oct-en-1-one and thiobarbituric acid reactive substances (TBARS), carbonyl, sulfhydryl, catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione S-transferase (GST), nitric oxide (NO) production and the release of the cytosolic enzyme lactate dehydrogenase (LDH) were measured. The organotellurium was not capable to alter TBARS and carbonyl assays. In contrast, the compound at 10 and 30 μM provoked a reduced of protein thiol groups measured by the sulfhydryl assay. Furthermore, the activity of the antioxidant enzyme CAT (10 and 30 μM) and GPx (1, 10 and 30 μM) was reduced by the organochalcogen. On the other hand, the activity of SOD and GST were enhanced respectively by 1, 10 and 30 μM of the compound. Furthermore, NO production was also increased by 30 μM of this organochalcogen. Finally, we verified that the organotellurium was capable of enhance the LDH release at 30 μM concentration. Our findings indicate that this organotellurium compound induces in vitro oxidative stress in the cerebral cortex of rats being potentially toxic for the brain of rats.     

Monensin potentiates lead chelation efficacy of MiADMSA in rat brain post chronic lead exposure

The present study evaluates combination therapy with a chelating agent, MiADMSA and a Na⁺ ionophore, monensin against sub-chronic lead toxicity in rats. Animals were exposed to 0.1% lead in drinking water for 16 weeks and then treated with either MiADMSA at 50 mg/kg body weight, or monensin at 10 mg/kg, or both in combination for a period of 5 days was administered. Biomarkers indicative of oxidative stress like ROS, GSH, GSSG and TBARS demonstrated lead-induced toxic manifestations in blood, kidney and brain. Antioxidants like SOD, catalase and glutathione peroxidase along with specific lead biomarker, blood ALAD were also severely depleted in lead intoxicated animals. Serum parameters and histopathological findings supported the said results. MiADMSA treatment during both mono- and combination therapy with monensin, restored the antioxidant status and recovered biochemical and haematological variables due to lead. However, monensin alone was not found to be effective in the given scenario. Interestingly, combination therapy in its ability to revert lead-induced overall systemic toxicity was only found at par with the MiADMSA monotherapy except for its chelation potential. Monensin given in combination with MiADMSA potentiated its lead chelation ability especially from brain, along with maintaining the normal copper concentrations in the organ unlike MiADMSA monotherapy.     

Influence of repeated preexposure to arsenic on acetaminophen-induced oxidative stress in liver of male rats

We evaluated whether repeated arsenic preexposure can increase acetaminophen-induced hepatic oxidative stress. Rats were exposed to arsenic (25 ppm; rat equivalent concentration of maximum groundwater contamination level) via drinking water for 28 days. Next day, they were given single oral administration of acetaminophen (420 or 1000 mg/kg b.w.). Hepatotoxicity was evaluated by assessing serum biomarkers, cytochrome-P450 (CYP) content, CYP3A4- and CYP2E1-dependent enzymes, lipid peroxidation and antioxidants. Arsenic or acetaminophen increased serum ALT and AST activities and depleted CYP. Arsenic decreased, but acetaminophen increased CYP-dependent enzyme activities. These agents independently increased lipid peroxidation and decreased antioxidants. Arsenic did not alter the effects of acetaminophen on serum biomarkers, caused further CYP depletion and decreased acetaminophen-mediated induction of drug-metabolizing enzymes. Arsenic enhanced the lower dose of acetaminophen-mediated lipid peroxidation and glutathione depletion with no further alterations in enzymatic antioxidants. However, arsenic attenuated the higher dose-mediated lipid peroxidation and glutathione depletion with improvement in glutathione peroxidase and glutathione reductase activities, further decrease in catalase and no alterations in superoxide dismutase and glutathione-S-transferase activities. Results show that arsenic preexposure increased the susceptibility of rats to hepatic oxidative stress induced by the lower dose of acetaminophen, but reduced the oxidative stress induced by the higher dose.     

Taurine suppresses doxorubicin-triggered oxidative stress and cardiac apoptosis in rat via up-regulation of PI3-K/Akt and inhibition of p53, p38-JNK

The objective of the present study was to investigate the signaling mechanisms involved in the beneficial role of taurine against doxorubicin-induced cardiac oxidative stress. Male rats were administered doxorubicin. Hearts were collected 3 weeks after the last dose of doxorubicin and were analyzed. Doxorubicin administration retarded the growth of the body and the heart and caused injury in the cardiac tissue because of increased oxidative stress. Similar experiments with doxorubicin showed reduced cell viability, increased ROS generation, intracellular Ca²⁺ and DNA fragmentation, disrupted mitochondrial membrane potential and apoptotic cell death in primary cultured neonatal rat cardiomyocytes. Signal transduction studies showed that doxorubicin increased p53, JNK, p38 and NFκB phosphorylation; decreased the levels of phospho ERK and Akt; disturbed the Bcl-2 family protein balance; activated caspase 12, caspase 9 and caspase 3; and induced cleavage of the PARP protein. However, taurine treatment or cardiomyocyte incubation with taurine suppressed all of the adverse effects of doxorubicin. Studies with several inhibitors, including PS-1145 (an IKK inhibitor), SP600125 (a JNK inhibitor), SB203580 (a p38 inhibitor) and LY294002 (a PI3-K/Akt inhibitor), demonstrated that the mechanism of taurine-induced cardio protection involves activation of specific survival signals and PI3-K/Akt as well as the inhibition of p53, JNK, p38 and NFκB. These novel findings suggest that taurine might have clinical implications for the prevention of doxorubicin-induced cardiac oxidative stress.     

A search for hepatoprotective activity of aqueous extract of Rhus coriaria L. against oxidative stress cytotoxicity

The protective effects of different concentrations of aqueous extract of Rhus coriaria L. fruit (75 and 100 μg/ml) and also gallic acid (100 μM) as one of its main components were examined against oxidative stress toxicity induced by cumene hydroperoxide (CHP) in isolated rat hepatocytes. Both extract concentrations and gallic acid (100 μM) significantly (P < 0.05) protected the hepatocyte against all oxidative stress markers including cell lysis, ROS generation, lipid peroxidation, glutathione depletion, mitochondrial membrane potential decrease, lysosomal membrane oxidative damage and cellular proteolysis. Aqueous extracts of Rhus coriaria L. (75 and 100 μg/ml) were more effective than gallic acid (100 μM) in protecting hepatocytes against CHP induced lipid peroxidation (P < 0.05). On the other hand gallic acid (100 μM) acted more effective than aqueous extracts of Rhus coriaria L. (75 and 100 μg/ml) at preventing hepatocyte membrane lysis (P < 0.05). In addition H₂O₂ scavenging effect of both extract concentrations (75 and 100 μg/ml) were determined in hepatocytes and compared with gallic acid (100 μM). Gallic acid (100 μM) was more effective than aqueous extracts of Rhus coriaria L. (75 and 100 μg/ml) at H₂O₂ scavenging activity (P < 0.05).     

The effects of vitamin A supplementation to rats during gestation and lactation upon redox parameters: Increased oxidative stress and redox modulation in mothers and their offspring

Vitamin A is an essential nutrient required in adequate amounts for reproduction and development. Subtle variations in the status of maternal nutrition may affect physiological and metabolic parameters in the fetus. Evidence suggests a key role for oxidative stress in these events. Literature is controversial about the effects of vitamin A supplementation. Here, we studied the effects of vitamin A supplementation on female Wistar rats during gestation and lactation on oxidative stress parameters of maternal and offspring tissues. Rats received daily doses of vitamin A at 2500, 12,500 and 25,000 IU/kg. We observed an increase of oxidative damage markers in the reproductive tissues and plasma of dams. The activity of glutathione-S-transferase was modulated by vitamin A supplementation. It was found to be increased in the liver of dams and decreased in the kidneys of mothers and offspring. In pups, supplementation decreased the total antioxidant potential of the liver along with decreased superoxide dismutase/catalase activity ratio in the kidney. The levels of lipoperoxidation were increased in male offspring, but decreased in female pups. Collectively, the results suggest that excessive vitamin A intake during gestation and lactation might be toxic for mothers with adverse effects for the developing offspring.     

4-hydroxynonenal induces mitochondrial oxidative stress, apoptosis and expression of glutathione S-transferase A4-4 and cytochrome P450 2E1 in PC12 cells

An excessive and sustained increase in reactive oxygen species (ROS) production and oxidative stress have been implicated in the pathogenesis of many diseases. In the present study, we have demonstrated that 4-hydroxynonenal (4-HNE), a product of lipid peroxidation, alters glutathione (GSH) pools and induces oxidative stress in PC12 cells in culture. This increase was accompanied by alterations in subcellular ROS and glutathione (GSH) metabolisms. The GSH homeostasis was affected as both mitochondrial and extramitochondrial GSH levels, GSH peroxidase and glutathione reductase activities were inhibited and glutathione S-transferase (GST) activity was increased after 4-HNE treatment. A concentration- and time-dependent increase in cytochrome P450 2E1 (CYP 2E1) activity in the mitochondria and postmitochondrial supernatant was also observed. 4-HNE-induced oxidative stress also caused an increase in the expression of GSTA4-4, CYP2E1 and Hsp70 proteins in the mitochondria. Increased oxidative stress in PC12 cells initiated apoptosis as indicated by the release of mitochondrial cytochrome c, activation of poly-(ADP-ribose) polymerase (PARP), DNA fragmentation and decreased expression of antiapoptotic Bcl-2 proteins. Mitochondrial respiratory and redox functions also appeared to be affected markedly by 4-HNE treatment. These results suggest that HNE-induced oxidative stress and apoptosis might be associated with altered mitochondrial functions and a compromised GSH metabolism and ROS clearance.     

Protective role of puerarin on lead-induced alterations of the hepatic glutathione antioxidant system and hyperlipidemia in rats

Puerarin (PU), a natural flavonoid, has been reported to have many benefits and medicinal properties. The aim of the present study was to investigate the effects of puerarin on hepatic oxidative stress and hyperlipidemia in rats exposed to lead. Our data showed that puerarin significantly prevented lead-induced hepatotoxicity, indicated by both diagnostic indicators of liver damage (serum aminotransferase levels) and histopathological analysis. Moreover, lead-induced profound elevation of ROS production and oxidative stress, as evidenced by increasing of lipid peroxidation level, reducing of GPx, GST, GR and GCL activities and depleting of intracellular reduced GSH level in liver, were suppressed by treatment with puerarin. Furthermore, the increase of serum cholesterol, triglycerides and LDL induced by lead was effectively suppressed by puerarin. The HDL level in the lead treatment rats was also increased by puerarin. Western blot analysis showed that puerarin remarkably inhibited hyperlipidemia by regulating the expression of cholesterol 7a-hydroxylase (CYP7A1), 3-hydroxy-3-methylglutaryl-CoA reductase (HMGR) and low-density lipoprotein receptor (LDL-R) in liver of lead treated rats. Altogether, these results suggest that puerarin could protect the lead-induced liver injury and hyperlipidemia by reducing ROS production, renewing the activities of antioxidant enzymes and influencing expression of hepatic lipid biosynthesis and metabolism genes.     

The influence of tobacco smoke exposure on selected markers of oxidative stress,kidneys and liver function in the serum of rats with streptozotocin-induced diabetes

BackgroundThe significance of the free radicals is emphasized in the pathophysiology of diabetes and the progression of chronic diabetic complications. Smoking cigarettes increases the risk of developing type II diabetes and intensifies pathophysiological processes during the development of type I diabetes. Tobacco smoke is also additional source of free radicals. Moreover, smoking causes variety of adverse effects on organs, that have no direct contact with the tobacco smoke itself. The objective of the study was to examine the effects of tobacco smoke on the serum concentrations of relevant oxidative stress markers such as total protein (TP), reduced glutathione (GSH), glutathione S-transferase (GST) and thiobarbituric acid reactive substances (TBARS), as well as renal (creatinine, urea) and liver function (alkaline phosphatase, ALP; alanine aminotransferase, ALT; aspartate aminotransferase, AST) among animals with induced diabetes after administration of a single dose of streptozotocin (65 mg/kg, ip).MethodsThe markers of oxidative stress and biochemical parameters were determined using spectrophotometric methods. As a biomarker of exposure to tobacco smoke, cotinine was determined using high-performance liquid chromatography with diode array detection (HPLC-DAD).ResultsTobacco smoke exposure of diabetic rats was manifested by significantly elevated liver enzymes activity - ALT (p < 0.05) and ALP (p < 0.01), higher creatinine and urea concentration (p < 0.01), lower GSH amount (p < 0.05), and higher GST activity (p < 0.05).ConclusionsTobacco smoking induce liver and renal damage through the mechanisms including increased oxidative stress.     

Protective effect of zinc supplementation against cadmium-induced oxidative stress and the RANK/RANKL/OPG system imbalance in the bone tissue of rats

It was investigated whether protective influence of zinc (Zn) against cadmium (Cd)-induced disorders in bone metabolism may be related to its antioxidative properties and impact on the receptor activator of nuclear factor (NF)-κΒ (RANK)/RANK ligand (RANKL)/osteoprotegerin (OPG) system. Numerous indices of oxidative/antioxidative status, and Cd and Zn were determined in the distal femur of the rats administered Zn (30 and 60 mg/l) or/and Cd (5 and 50 mg/l) for 6 months. Soluble RANKL (sRANKL) and OPG were measured in the bone and serum. Zn supplementation importantly protected from Cd-induced oxidative stress preventing protein, DNA, and lipid oxidation in the bone. Moreover, Zn protected from the Cd-induced increase in sRANKL concentration and the sRANKL/OPG ratio, and decrease in OPG concentration in the bone and serum. Numerous correlations were noted between indices of the oxidative/antioxidative bone status, concentrations of sRANKL and OPG in the bone and serum, as well as the bone concentrations of Zn and Cd, and previously reported by us in these animals (Brzóska et al., 2007) indices of bone turnover and bone mineral density. The results allow us to conclude that the ability of Zn to prevent from oxidative stress and the RANK/RANKL/OPG system imbalance may be implicated in the mechanisms of its protective impact against Cd-induced bone damage. This paper is the first report from an in vivo study providing evidence that beneficial Zn impact on the skeleton under exposure to Cd is related to the improvement of the bone tissue oxidative/antioxidative status and mediating the RANK/RANKL/OPG system.     

The methanolic fraction of Centratherum anthelminticum seed downregulates pro-inflammatory cytokines,oxidative stress,and hyperglycemia in STZ-nicotinamide-induced type 2 diabetic rats

This study aimed to ascertain the potential of Centratherum anthelminticum seeds methanolic fraction (CAMFs) for the management of type 2 diabetes and its associated complications. CAMFs was initially tested on β-TC6 cells for H₂O₂-induced nuclear factor-κB (NF-κB) translocation effects. The result displayed that CAMFs significantly inhibited NF-κB translocation from cytoplasm into the nucleus, dose-dependently. Furthermore, a 12-week sub-chronic CAMFs study was carried out on streptozotocin (STZ)-nicotinamide–induced type 2 diabetic rat model to evaluate glycemia, essential biochemical parameters, lipid levels, oxidative stress markers, and pro-inflammatory cytokines level. Our study result showed that CAMFs reduced hyperglycemia by increasing serum insulin, C-peptide, total protein, and albumin levels, significantly. Whereas, elevated blood glucose, glycated hemoglobin, lipids and enzyme activities were restored to near normal. CAMFs confirmed antioxidant potential by elevating glutathione (GSH) and reducing malondialdehyde (MDA) levels in diabetic rats. Interestingly, CAMFs down-regulated elevated tumor necrosis factor α (TNF-α), interleukin (IL)-1β and IL-6 in the tissues and serum of the diabetic rats. We conclude that CAMFs exerted apparent antidiabetic effects and demonstrated as a valuable candidate nutraceutical for insulin-resistant type 2 diabetes and its associated complications such as dyslipidemia, oxidative stress, and inflammation.