Aged black garlic extract inhibits HT29 colon cancer cell growth via the PI3K/Akt signaling pathway

Ma, Dong; Yang, Guliang; Liu, Hanchen; Liu, Xiaoxu; Lin, Shiji; Sun, Di; Wang, Yishan

doi:10.3892/br.2014.226

Cited by 92 publications

(74 citation statements)

References 20 publications

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“…The PI3K/Akt signaling pathway is involved in cell differentiation, proliferation, apoptosis and migration, and excessive activation of this pathway leads to cell dysfunction (26). A previous study indicated that PI3K/Akt signaling pathway activation occurs in association with DN, and high sugar or transforming growth factor-β1 levels can cause changes to certain podocyte proteins such as ZO-1 and CD2AP by activating this pathway (27).…”

Section: Discussionmentioning

confidence: 99%

Renoprotective effects of emodin against diabetic nephropathy in rat models are mediated via PI3K/Akt/GSK‑3β and Bax/caspase‑3 signaling pathways

2017

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Abstract. Emodin is the main active component of the Chinese medicine rhubarb, which has a variety of pharmacological effects and a high clinical value. Its anti-inflammatory and antitumor effects have been widely studied. The aim of the present study was to determine whether emodin has renoprotective effects, and to identify the potential underlying mechanisms in a rat model of diabetic nephropathy (DN). The changes in mean blood glucose levels, normalized kidney weight, urinary albumin excretion, serum creatinine levels and tubulointerstitial injury index (TII) scores of the rats with DN were significantly attenuated by emodin. Furthermore, treatment with emodin significantly inhibited inflammation-related factors and oxidative stress, suppressed the expression of intercellular adhesion molecule 1 (ICAM-1) and B-cell lymphoma 2-associated X protein (Bax), increased phosphorylated Akt and phosphorylated-glycogen synthase kinase 3 (p-GSK-3β) expression and inhibited caspase-3 activity in diabetic rats. These data suggest that emodin protects against DN and that the underlying mechanism may involve the suppression of inflammation, ICAM-1 and Bax, and activation of the PI3K/Akt/GSK-3β pathway.

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Section: Discussionmentioning

confidence: 99%

Renoprotective effects of emodin against diabetic nephropathy in rat models are mediated via PI3K/Akt/GSK‑3β and Bax/caspase‑3 signaling pathways

2017

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“…As an inhibitor of PI3K can block the activation of Akt, the activation status of PI3K/Akt pathways can be predicted by observing the expression of p-Akt (10). Previous results have suggested that apoptosis plays an important role in cerebral neuron death after epilepsy (31). As a key component of survival signal, Akt is necessary to cellular survival triggered by growth factors, extra-cellular matrix and other stimulus (31).…”

Section: Discussionmentioning

confidence: 99%

“…Previous results have suggested that apoptosis plays an important role in cerebral neuron death after epilepsy (31). As a key component of survival signal, Akt is necessary to cellular survival triggered by growth factors, extra-cellular matrix and other stimulus (31). Activated Akt is a cellular survival factor that can help cells escape from programmed cell death by inactivating multiple effector molecules of apoptosis (32).…”

Section: Discussionmentioning

confidence: 99%

Geniposide attenuates epilepsy symptoms in a mouse model through the PI3K/Akt/GSK‑3β signaling pathway

Wei¹,

Duan²,

He³

et al. 2017

Exp Ther Med

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Abstract. Previous reports on the pharmacological actions of geniposide have indicated that it has anti-asthmatic, anti-inflammatory and analgesic effects in the liver and gallbladder, and therapeutic effects in neurological, cardiovascular and cerebrovascular diseases. The results of the current study demonstrate that geniposide attenuates epilepsy in a mouse model through the phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt)/glycogen synthase kinase-3β (GSK-3β) signaling pathway. A mouse model of epilepsy was induced by maximal electric shock (50 mA, 50 Hz, 1 sec). Epilepsy mice were intragastrically administered with 0, 5, 10 or 20 mg/kg geniposide. Geniposide significantly reduced the incidence and significantly increased the latency of clonic seizures in epileptic mice compared with non-treated epileptic mice (both P<0.01). Geniposide treatment significantly inhibited cyclooxygenase-2 mRNA expression in epilepsy mice (P<0.01). Furthermore, geniposide significantly suppressed the protein expression of activator protein 1, increased the activation of Akt and increased the protein expression of GSK-3β and PI3K in epilepsy mice (all P<0.01). These results suggest that geniposide attenuates epilepsy in mice through the PI3K/Akt/GSK-3β signaling pathway.

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“…Azoxymethane (AOM), the oxide of azomethane, is procarcinogenic that induces colon cancer in rats and mice ( Escribano et al, 2004 andDong et al, 2014). AOM induces colon cancer via mechanisms that include glutathione depletion and impairing total antioxidant capacity so inducing oxidative stress in colonic cells of rats (Waly et al, 2012).…”

Section: Discussionmentioning

confidence: 99%

“…AOM is a strong inducer of precancerous and dysplastic lesions (aberrant crypt foci, (ACF) in rodent colon and is particularly effective for the induction of colon adenocarcinoma (Dong et al, 2014). In addition, Venning et al, (2013) concluded that Azoxymethane (AOM) enhances early inflammation-induced colon crypt pathology in mice.…”

Section: Introductionmentioning

confidence: 99%

Anticancer Effect of Black Raspberry and Apricot Juice against Colon Cancer Induced by Azoxymethane in Male Rats

Ibrahim¹

2017

Int. J. Adv. Res. Biol. Sci

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This study was carried out to evaluate the anticancer effect of black raspberry juice (RJ) and apricot juice (AJ) against colon cancer induced by Azoxymethane (AOM) in rats and to examine the possible mechanisms. Forty two Sprague Dawley male rats were used and randomly distributed into 6 equal groups (n=7). The 1 st group was negative control and each rat from the other 5 groups was given a single subcutaneous dose (15 mg/kg b.wt.) of AOM once weekly for 2 weeks to induce colon cancer. The 2 nd group was kept positive control and rats in the 3 rd , 4 th , 5 th and 6 th groups were orally given RJ and AJ at low (5%) and high (10%) concentrations, respectively, daily for 12 weeks. Serum colon cancer biomarkers [(tumor necrosis factor α-(TNF-α); nuclear factor-κappaB (NF-κB); interleukin1β (IL-1β) and interleukin and 6 (IL6)] were measured and histopathology of the colon was done to evaluate the anticancer effect. Lipid peroxidation and activities of antioxidant enzymes in colon tissues and content of 8-hydroxy-2-deoxyguanosine (8-OHdG) (apoptosis marker) in colon DNA were measured to examine the possible mechanisms. The results showed that oral administration of RJ and AJ inhibited AOM-induced elevations in serum colon cancer biomarkers levels, antagonized preneoplastic abbrent colon crypts induced by AOM, decreased lipid peroxidation; increased activities of antioxidant enzymes in colon tissues and reduced elevation of 8-OHdG content in colon DNA. These results denoted that RJ and AJ have an anticancer effect against colon cancer. The mechanistic studies demonstrated that RJ and AJ inhibited lipid peroxidation, increased antioxidant enzyme activities (antagonized oxidative stress) and induced of apoptosis. It can be concluded that intake of black raspberry and apricot as fruit salad or juice may be beneficial for patients who suffer from colon cancer.

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Aged black garlic extract inhibits HT29 colon cancer cell growth via the PI3K/Akt signaling pathway

Cited by 92 publications

References 20 publications

Renoprotective effects of emodin against diabetic nephropathy in rat models are mediated via PI3K/Akt/GSK‑3β and Bax/caspase‑3 signaling pathways

Renoprotective effects of emodin against diabetic nephropathy in rat models are mediated via PI3K/Akt/GSK‑3β and Bax/caspase‑3 signaling pathways

Geniposide attenuates epilepsy symptoms in a mouse model through the PI3K/Akt/GSK‑3β signaling pathway

Anticancer Effect of Black Raspberry and Apricot Juice against Colon Cancer Induced by Azoxymethane in Male Rats

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