Asarone and metformin delays experimentally induced hepatocellular carcinoma in diabetic milieu

Das, Bhrigu Kumar; Choukimath, S. M.; Gadad, Pramod C.

doi:10.1016/j.lfs.2019.05.046

Cited by 15 publications

(12 citation statements)

References 37 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The results of this study suggest that metformin and asarone suppress the hepatic cancer cell viability and arrested the cell cycle at the G 0 /G 1 phase by AMPK activation and Akt inhibition. Studies, including our own, suggest that higher blood glucose concentration may be associated with the increased risk of cancers [23,[30][31][32][33]. The increased proliferation of HepG2 cells at elevated glucose levels may be due to glucose toxicity resulting from increased production of reactive oxygen species (ROS) and alteration in the expression of genes [4,34].…”

Section: Discussionmentioning

confidence: 99%

“…On the other hand, alpha (α)-and beta (β)-asarone, the two major active constituents in volatile oils of Acorus calamus, showed anti-cancer effects in various cancer cell lines [21,22]. Our previous study showed that asarone treatment attenuated the progression of HCC in diabetic conditions in a similar manner to that achieved by metformin [23]. The present study was aimed to understand whether the anti-proliferative effect of asarone is mediated via AMPK and Akt signaling pathway similar to the metformin, which was used as a reference drug.…”

Section: Introductionmentioning

confidence: 88%

See 1 more Smart Citation

Metformin and asarone inhibit HepG2 cell proliferation in a high glucose environment by regulating AMPK and Akt signaling pathway

2021

Self Cite

View full text Add to dashboard Cite

Background Metabolic dysregulation is one of the hallmarks of tumor cell proliferation. Evidence indicates the potential role of the 5′adenosine monophosphate-activated protein kinase (AMPK) and protein kinase B/Akt signaling pathway in regulating cell proliferation, survival, and apoptosis. The present study explores the effect of metformin HCl and the combination of α- and β-asarone on the proliferation of HepG2 cells in the presence of high glucose levels simulating the diabetic-hepatocellular carcinoma (HCC) condition. Results The metformin and asarone reduced HepG2 cell viability in a dose-dependent manner and induced morphological changes as indicated by methyl thiazolyl tetrazolium (MTT) assay. The metformin and asarone arrested the cells at the G0/G1 phase, upregulated the expression of AMPK, and downregulated Akt expression in high glucose conditions as identified by the flow cytometry technique. Further, the upregulated AMPK led to a decrease in the expression of phosphoenolpyruvate carboxykinase-2 (PCK-2) and sterol regulatory element-binding protein-1 (SREBP-1). Conclusion The anti-proliferative effect of metformin and asarone in the diabetic-HCC condition is mediated via AMPK and Akt pathway.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 88%

Metformin and asarone inhibit HepG2 cell proliferation in a high glucose environment by regulating AMPK and Akt signaling pathway

2021

Self Cite

View full text Add to dashboard Cite

show abstract

“…The effect of STZinstigating hyperglycaemia on the development of HCC following a single injection of DEN in experimental rats unveiled all the characteristic features of diabetes and hepatocarcinogenesis as confirmed in our previous study. 14 The diabetic liver is strongly correlated with the increased possibility of HCC by 2.5 folds as observed by some studies in contrast with their non-diabetic counterparts. 23,24 The involvement of the free radicalsmediated oxidative stress during hyperglycaemic condition has been involved in the pathological process and progress of diabetes and it contributes to damage to various tissues and organs, including the liver.…”

Section: Discussionmentioning

confidence: 90%

“…[11][12][13] Our earlier study reported that asarone treatment decreased the development of HCC in a hyperglycaemic condition comparable to metformin. 14 Considering the above fact that the altered cellular oxidative stress is responsible and also shared as a causal factor between both the diseases, however, there is no evidence related to asarone to support their protection against oxidative stress-induced damage in diabetic-HCC condition. Therefore, the present investigation evaluated the efficacy of asarone and metformin HCl in maintaining the balance in the oxidant-antioxidant status during the diabetic-HCC condition in male Wistar rats.…”

Section: Introductionmentioning

confidence: 99%

Asarone and Metformin Modulates the Oxidant- Antioxidant Imbalance on Experimentally Induced Hepatocellular Carcinoma during Diabetic Condition

Das¹,

Gadad²

2020

IJPER

Self Cite

View full text Add to dashboard Cite

“…Activity [16] The scavenging was estimated using nitroblue tetrazolium (NBT) as given by Sabu and Ramadas an (2002). Different concentrations of extract (10-320 μg/ml) were taken in a test tube.…”

Section: Estimation Of Superoxide Radical-scavengingmentioning

confidence: 99%

Untitled

Sharma¹

2019

IJGP

View full text Add to dashboard Cite

Aim: The present study was designed to investigate the effect of different extracts of Excoecaria agallocha L. in the treatment of diabetes and its complications. Diabetes was induced by intraperitoneal administration of streptozotocin (65 mg/kg) for the development of diabetic nephropathy and neuropathy. Diabetic nephropathy was evaluated by assessing levels of fasting blood glucose, glycated hemoglobin (Hb A1C), serum insulin level, albuminuria, serum urea, uric acid, creatinine, and blood urea nitrogen along with altered lipid profile (total cholesterol, triglycerides, low-density lipoprotein [LDL], very LDL, and high-density lipoprotein-cholesterol). Materials and Methods: Oral treatment of diabetic rats with extracts of E. agallocha L. improved renal dysfunction indicated by a significant decrease in urinary albumin; serum creatinine, urea, and uric acid. Moreover, a significant increase in body weight along with a significant decrease in fasting blood glucose and Hb A1C in treated groups was observed. Hyperglycemia-induced oxidative stress in diabetic control rats indicated by a significant decrease in superoxide dismutase and reduced glutathione level with a significant increase in malondialdehyde (thiobarbituric acid reactive substances) levels was also ameliorated by treatment with extracts. Results and Discussion: Development of neuropathy was evident from marked hyperalgesia (thermal as well as mechanical) and tactile allodynia along with reduced Motor nervous conduction velocity (MNCV). An elevated level of nitrite, tumor necrosis factor-α (TNF-α), transforming growth factor-β (TGF-β), and interleukin-1β (IL-1β) were also assessed in the sciatic nerve of diabetic neuropathy animals. Treatment with different extracts of E. agallocha L. significantly attenuated elevated thermal and mechanical hyperalgesia. Elevated tactile allodynia assessed using flexible Von Frey filaments was also reversed by extracts. Treatment with both extracts significantly attenuated the parameters of oxidative stress in sciatic nerve of diabetic neuropathy rats. Furthermore, level of nitrite, TNF-α, TGF-β, and IL-1β significantly increased in the sciatic nerve of diabetic neuropathy animals that were ameliorated by treatment with E. agallocha L. extracts. Conclusion: Histopathological changes in kidney, pancreas, liver, and sciatic nerve of diabetic rats were also reversed by the treatment. These findings suggested that treatment with E. agallocha L. ameliorated diabetes and its complications (diabetic nephropathy and diabetic neuropathic pain).

show abstract

Asarone and metformin delays experimentally induced hepatocellular carcinoma in diabetic milieu

Cited by 15 publications

References 37 publications

Metformin and asarone inhibit HepG2 cell proliferation in a high glucose environment by regulating AMPK and Akt signaling pathway

Metformin and asarone inhibit HepG2 cell proliferation in a high glucose environment by regulating AMPK and Akt signaling pathway

Asarone and Metformin Modulates the Oxidant- Antioxidant Imbalance on Experimentally Induced Hepatocellular Carcinoma during Diabetic Condition

Untitled

Contact Info

Product

Resources

About