Hispidin
Hispidin exhibits anti-inflammatory activity through suppressing ROS mediated NF-κB pathway in mouse macrophage cells, it also has anti-cancer activity by inducing both intrinsic and extrinsic apoptotic pathways mediated by ROS in colon cancer cells. Hispidin can inhibit Acrylamide-induced oxidative stress and protect C2C12 myotubes against palmitate-induced oxidative stress by suppressing cleavage of caspase-3, expression of Bax, and NF-κB translocation.
Hispidin protects against apoptosis in H9c2 cardiomyoblast cells exposed to hydrogen peroxide through reducing intracellular ROS production, regulating apoptosis-related proteins, and the activation of the Akt/GSK-3β and ERK1/2 signaling pathways.
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Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to
24 months(2-8C).
Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.
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Exp Cell Res. 2014 Oct 1;327(2):264-75.
The protective effect of hispidin against hydrogen peroxide-induced apoptosis in H9c2 cardiomyoblast cells through Akt/GSK-3β and ERK1/2 signaling pathway.[Pubmed:
25128810]
Hispidin, a phenolic compound from Phellinus linteus (a medicinal mushroom), has been shown to possess strong anti-oxidant, anti-cancer, anti-diabetic, and anti-dementia properties. However, the cardioprotective efficacy of Hispidin has not yet been investigated.
METHODS AND RESULTS:
In the present study, we investigated the protective effect of Hispidin against oxidative stress-induced apoptosis in H9c2 cardiomyoblast cells and neonatal rat ventricular myocytes. While the treatment of H9c2 cardiomyoblast cells with hydrogen peroxide caused a loss of cell viability and an increase in the number of apoptotic cells, Hispidin significantly protected the cells against hydrogen peroxide-induced cell death without any cytotoxicity as determined by XTT assay, LDH release assay, Hoechst 33342 assay, and Western blotting of apoptosis proteins such as caspase-3, Bax, and Bcl-2. Our data also shows that Hispidin significantly scavenged intracellular ROS, and markedly enhanced the expression of antioxidant enzymes such as heme oxygenase-1 and catalase, which was accompanied by the concomitant activation of Akt/GSK-3β and ERK1/2 phosphorylation in H9c2 cardiomyoblast cells. The effects of Hispidin on Akt and ERK phosphorylation were abrogated by LY294002 (a PI3K/Akt inhibitor) and U0126 (an ERK1/2 inhibitor). The effect of Hispidin on GSK-3b activities was also blocked by LY294002. Furthermore, inhibiting the Akt/GSK-3β and ERK1/2 pathway by these inhibitors significantly reversed the Hispidin-induced Bax and Bcl-2 expression, apoptosis induction, and ROS production.
CONCLUSIONS:
These findings indicate that Hispidin protects against apoptosis in H9c2 cardiomyoblast cells exposed to hydrogen peroxide through reducing intracellular ROS production, regulating apoptosis-related proteins, and the activation of the Akt/GSK-3β and ERK1/2 signaling pathways.
J Sci Food Agric. 2014 Oct 30.
Anti-inflammatory activity of mushroom-derived hispidin through blocking of NF-κB activation.[Pubmed:
25355452]
Hispidin, a polyphenol compound mainly derived from the valuable medicinal mushroom Phellinus species, has been found to possess distinct biological effects. However, the anti-inflammatory potential of Hispidin still remains uncharacterized.
METHODS AND RESULTS:
In this study, the effects of Hispidin on activation of nuclear factor kappa B (NF-κB) and the subsequent production of inducible nitric oxide synthase (iNOS) were determined in the lipopolysaccharide (LPS)-induced macrophage RAW 264.7 cells. Our data indicated that Hispidin inhibits transcriptional activity of NF-κB in a dose-dependent manner. Hispidin also attenuated LPS-induced NF-κB nuclear translocation and associated inhibitor of kappa B (IκB-α) degradation. Furthermore, Hispidin deceased iNOS protein expression and the generation of reactive oxygen species (ROS) in the LPS-induced cells, but did not affect phosphorylation of mitogen-activated protein kinases.
CONCLUSIONS:
These findings suggest that Hispidin exhibits anti-inflammatory activity through suppressing ROS mediated NF-κB pathway in mouse macrophage cells.
Chem Biol Interact. 2014 Aug 5;219:83-9.
Hispidin derived from Phellinus linteus affords protection against acrylamide-induced oxidative stress in Caco-2 cells.[Pubmed:
24877638]
METHODS AND RESULTS:
Hispidin produced from the edible fungus Phellinus linteus displayed dramatically antioxidant activities against DPPH radicals, ABTS radicals, ferric reducing and hydroxyl radicals, as well as superoxide anion radicals. Moreover, the cytoprotective effect of Hispidin against AA-induced oxidative stress was verified upon Caco-2 cells according to evaluate the cell viability, intracellular ROS, mitochondrial membrane potential (MMP) and glutathione (GSH) in the presence or absence of AA (5 mM) in a dose-dependent manner.
CONCLUSIONS:
Collectively, our results demonstrated for the first time that Hispidin was able to inhibit AA-induced oxidative stress, which might have implication for the dietary preventive application.
Anticancer Res. 2014 Aug;34(8):4087-93.
Anticancer activity of hispidin via reactive oxygen species-mediated apoptosis in colon cancer cells.[Pubmed:
25075033]
Few studies have been performed on the anticancer activity of Hispidin, a phenolic compound produced from the medicinal mushroom Phellinus linteus.
METHODS AND RESULTS:
Herein, we studied Hispidin-induced apoptosis, which is associated with the generation of reactive oxygen species (ROS) in colon cancer cells. Hispidin was found to reduce cell viability both in mouse and human colon cancer cells. Apoptotic cell morphological changes were observed by microscopy, and apoptosis was assessed in Hispidin-treated cells using a biochemical method. The results showed accumulation of the sub-G1 cell population and increase in early apoptosis in a dose-dependent manner. In addition, Hispidin induced apoptosis through up-regulation of both intrinsic and extrinsic apoptotic pathways. Although the molecular mechanism underlying Hispidin-induced apoptosis is known to involve the generation of ROS, however Hispidin did not show any apoptosis in the pre-treatment with a ROS scavenger, N-acetyl-L-cysteine.
CONCLUSIONS:
In conclusion, Hispidin induces both intrinsic and extrinsic apoptotic pathways mediated by ROS in colon cancer cells, thereby suggesting that Hispidin could be a promising new anticancer agent.
Molecules. 2015 Mar 27;20(4):5456-67.
Cytoprotective effect of hispidin against palmitate-induced lipotoxicity in C2C12 myotubes.[Pubmed:
25826786]
It is well known that Phellinus linteus, which produces Hispidin and its derivatives, possesses antioxidant activities.
METHODS AND RESULTS:
In this study, we investigated whether Hispidin has protective effects on palmitate-induced oxidative stress in C2C12 skeletal muscle cells. Our results showed that palmitate treatment in C2C12 myotubes increased ROS generation and cell death as compared with the control. However, pretreatment of Hispidin for 8 h improved the survival of C2C12 myotubes against palmitate-induced oxidative stress via inhibition of intracellular ROS production. Hispidin also inhibited palmitate-induced apoptotic nuclear condensation in C2C12 myotubes. In addition, we found that Hispidin can suppress cleavage of caspase-3, expression of Bax, and NF-κB translocation.
CONCLUSIONS:
Therefore, these results suggest that Hispidin is capable of protecting C2C12 myotubes against palmitate-induced oxidative stress.
