All our mushroom cultures are only one to two transfers away from the 1st generation mother culture to ensure a vibrant, healthy, and fast-growing product.
Each liquid mushroom culture syringe contains 12 cc's of mycelium suspended in a nutrient broth solution or commonly referred to as a liquid culture. Unlike many vendors, our cultures do not contain honey, we use a special clear recipe so you can see exactly what you're getting. Your mushroom culture is guaranteed to arrive 100% viable and completely contamination-free ready to inoculate a substrate of your choice.
You may use your LC Syringe right away, or store it in its mylar container in the refrigerator for 6 months or longer!
Your order with us today will contain:
(1) sterile 12 ml syringe with locking cap and selected strain.
(1) mylar syringe sleeve for long-term storage.
(2) alcohol pads.
(1) 18 gauge needle.
WE SHIP EVERYWHERE
Worldwide shipping makes us the most turned to mushroom culture producer/distributor in the world. If you canï¾’t find it in your country, we have you covered and our shipping time is considerably less than what you may expect.
Ferulae Mushroom Pleurotus Ferulae
Pleurotus ferulae is a kind of editable mushroom and has various biological functions such as antitumor, antioxidation and immunoregulation. Wild P. ferulae was successfully domesticated but the antitumor function and mechanisms of cultivated and wild P. ferulae need to be compared and explored. Here, we prepared cultivated and wild P. ferulae ethanol extracts (PFEE-C and PFEE-W) and compared their antitumor effect on hepatocellular carcinoma. Our data showed that PFEE-C and PFEE-W significantly inhibited the growth of H22 and HepG2 cells through induction of apoptosis. PFEE-W exhibited higher antitumor activity than PFEE-C. Both PFEE-C and PFEE-W induced endoplasmic reticulum (ER) stress characterized by the up-regulated levels of phosphorylated JNK, cleaved caspase-12 and HSP70, and mitochondrial dysfunction characterized by the reduction of mitochondrial membrane potential and the release of cytochrome c, which promoted the cleavage of caspase-3, -7, -9 and PARP. Moreover, PFEE-C and PFEE-W significantly increased ROS generation in H22 cells and suppressed H22 cell migration through reducing the levels of matrix metalloproteinase -2 and -9. Further, PFEE-C inhibited H22 tumor growth in mouse model and improved the survival of tumor mice. These results indicated that PFEE-C and PFEE-W could inhibit hepatocellular carcinoma cell growth through ER stress- and mitochondria-dependent apoptotic pathways.
Liver cancer, which consists predominantly of hepatocellular carcinoma (HCC), ranks the sixth for cancer incidence and the fourth for cancer mortality worldwide1. The highest incidence and mortality rates of HCC were found in East Asia and central sub-Saharan Africa1, which resulted from chronic infection with hepatitis virus and other factors including food- and water-borne carcinogens2. In 2015, the estimated new liver cancer cases are 466,100 and the estimated deaths are 422,100 in China3. Currently, the treatments of liver cancer include surgery, targeted therapy, radiotherapy, chemotherapy, or their combinations4,5,6,7,8. However, the clinical efficacy is still unsatisfied. It definitively needs to develop safe and effective drugs for treating liver cancer.
Accumulating evidence has shown that edible mushrooms have many biological activities and have been used as a source of natural medicine and functional food9,10. Pleurotus ferulae is an edible mushroom and grows on the living rhizome trunks of Ferula asafoetida in the Gobi desert, which is mainly distributed in Xinjiang, China11. Several studies including ours have reported that P. ferulae has anti-tumor, anti-microbial, anti-oxidant and immunomodulatory functions11,12,13,14,15,16. It has been shown that the cytotoxicity of P. ferulae ethanol extract is higher than that of hot water extract on several human cancer cell lines and can induce the synergistic effects on the TRAIL-induced apoptosis in A549 cells17. Our previous study also showed that P. ferulae ethanol extract (PFEE) inhibited the growth of melanoma cell line B16F10 in vitro and in vivo through induction of cell cycle arrest and mitochondria-mediated apoptosis11. Due to the limit resource and important values in nutrition and pharmacology, wild P. ferulae was successfully domesticated by Xinjiang Institute of soil biological desert in 1990. Whether wild and/or cultivated P. ferulae have antitumor effect on HCC and the difference of their antitumor effect on HCC are still elusive.
In this study, we prepared ethanol extracts of cultivated and wild P. ferulae and named as PFEE-C and PFEE-W, respectively. The antitumor effects of PFEE-C and PFEE-W on HCC were detected and compared in H22 and HepG2 cells. We found that both PFEE-C and PFEE-W could inhibit the growth of H22 and HepG2 cells through induction of apoptosis, which was mediated by mitochondria-dependent and endoplasmic reticulum (ER) stress-dependent pathways in H22 cells. The results indicated that PFEE might be used to develop antitumor drugs against HCC.
PFEE-C and PFEE-W inhibit the growth of H22 and HepG2 cells in vitro
The ethanol extractions of cultivated and wild P. ferulae were prepared and named as PFEE-C and PFEE-W. Their flavonoid contents are 1.37% and 1.5%, respectively. To investigate the antitumor effect of PFEE, H22 and HepG2 cells were treated with different concentrations of PFEE-C and PFEE-W according to their flavonoid contents. After 24?h, the morphology of H22 cells was observed by microscope and it was significantly changed by PFEE-C and PFEE-W treatment in a dose-dependent manner (Fig. 1a). The similar changes of cell morphology were observed in HepG2 cells (Supplemental Fig. 1a). The viability of H22 and HepG2 cells was measured by MTT assay at the indicated time points. As shown in Fig. 1b, both PFEE-C and PFEE-W were significantly reduced the viability of H22 cells in a dose- and time-dependent manner compared to control (p?<?0.001). Moreover, the inhibitory activity of PFEE-W was significantly higher than that of PFEE-C on H22 cells after 24?h and 72?h (Fig. 1b). Similar cytotoxicity of PFEE-C and PFEE-W were observed in HepG2 cells (Supplemental Fig. 1b). The inhibition rates of 5.472 and 8.208?µg/ml flavonoids in PFEE-C and PFEE-W on H22 cells were higher than 50% and 60%, respectively, after 72?h treatment. We also detected the effect of PFEE on the proliferation of murine splenocytes. The results showed that both PFEE-C and PFEE-W significantly increased the proliferation of splenocytes (p?<?0.01). PFEE-W showed stronger activity on splenocyte proliferation than PFEE-C at 8.208?µg/ml flavonoids (Fig. 1c). These results suggested that PFEE-C and PFEE-W inhibited H22 and HepG2 cell growth in a dose-dependent and time-dependent manner, but they had no cytotoxic effect on splenocytes.