Potential Fungi Isolated From Anti-biodegradable Chinese Medicine Residue to Degrade Lignocellulose.

Traditional Chinese medicine is one of the ancient medicines which is popular in Asian countries, among which the residue produced by the use of anti-biodegradables is endless, and causes significant adverse impacts on the environment. However, the high acidity of anti-biodegradable residues and some special biological activities make it difficult for microorganisms to survive, resulting in a very low degradation rate of lignocellulose in naturally stacked residues, which directly impedes the degradation of residues. We aimed to identify the fungal strains that efficiently biodegrade anti-biodegradable residue and see the possibility to improve the biodegradation of it and other agricultural wastes by co-cultivating these fungi. We isolated 302 fungal strains from anti-biodegradable residue to test hydrolysis ability. Finally, we found Coniochaeta sp., Fomitopsis sp., Nemania sp., Talaromyces sp., Phaeophlebiopsis sp. which inhabit the anti-biodegradable residues are capable of producing higher concentrations of extracellular enzymes. Synergistic fungal combinations (viz., Fomitopsis sp. + Phaeophlebiopsis sp.; Talaromyces sp. + Coniochaeta sp. + Fomitopsis sp.; Talaromyces sp. + Fomitopsis sp. + Piloderma sp. and Talaromyces sp. + Nemania sp. + Piloderma sp.) have better overall degradation effect on lignocellulose. Therefore, these fungi and their combinations have strong potential to be further developed for bioremediation and biological enzyme industrial production.

Protective effect of Terminalia chebula Retz. extract against Aß aggregation and Aß-induced toxicity in Caenorhabditis elegans.

ETHNOPHARMACOLOGICAL RELEVANCE: Terminalia chebula Retz. (T.chebula) is an important medicinal plant in Tibetan medicine and Ayurveda. T.chebula is known as the "King of Tibetan Medicine", due to its widespread clinical pharmacological activity such as anti-inflammatory, antioxidative, antidiabetic as well as anticancer in lots of in vivo and in vitro models. In this study, we use transgenic and/or RNAi Caenorhabditis elegans (C.elegans) model to simulation the AD pathological features induced by Aß, to detect the effect of TWE on improving Aß-induced toxicity and the corresponding molecular mechanism. AIM OF STUDY: The study aimed to tested the activities and its possible mechanism of T.chebula to against Aß1-42 induced toxicity and Aß1-42 aggregation. MATERIALS AND METHODS: Using transgenic C.elegans strain CL2006 and CL4176 as models respond to paralytic induced by Aß toxicity. The transcription factors DAF-16 and SKN-1 were analyzed used a fluorescence microscope in transgenic strains (DAF-16:GFP, SKN-1:GFP). The function of DAF-16 and SKN-1 was further investigated using loss-of-function strains by feeding RNA interference (RNAi) bacteria. To evaluate the aggregation level of Aß in the transgenic C.elegans, Thioflavin S (ThS) staining and WB visualized the levels of Aß monomers and oligomers. RESULTS: TWE treatment can significantly improve the paralysis of transgenic C.elegans caused by Aß aggregation (up to 14%). The Aß aggregates in transgenic C.elegans are significantly inhibited under TWE exposure (up to 70%). TWE increases the nuclear localization of the key transcription factor DAF-16 and HSF-1, which in turn leads to the expression of downstream Hsp-16.2 protein and exerts its inhibitory effect on Aß aggregation. Meanwhile, paralysis improved has not observed in SKN-1 mutation and/or RNAi C.elegans. CONCLUSION: Our results indicate that TWE can protect C.elegans against the Aß1-42-induced toxicity, inhibition Aß1-42 aggregation and delaying Aß-induced paralysis. The neuroprotective effect of TWE involves the activation of DAF-16/HSF-1/Hsp-16.2 pathway.

Dianxianning improved amyloid ß-induced pathological characteristics partially through DAF-2/DAF-16 insulin like pathway in transgenic C. elegans.

Dianxianning (DXN) is a traditional Chinese formula, and has been approved in China for treating epilepsy since 1996. Here anti-Alzheimer's disease activity of DXN has been reported. DXN improved AD-like symptoms of paralysis and 5-HT sensitivity of transgenic Aß1-42 C. elegans. In worms, DXN significantly increased Aß monomers and decreased the toxic Aß oligomers, thus reducing Aß toxicity. DXN significantly suppressed the expression of hsp-16.2 induced by juglone, and up-regulated sod-3 expression. These results indicated that DXN increased stress resistance and protected C. elegans against oxidative stress. Furthermore, DXN could significantly promote DAF-16 nuclear translocation, but it did not activate SKN-1. The inhibitory effect of DXN on the Aß toxicity was significantly reverted by daf-16 RNAi, rather than skn-1 RNAi or hsf-1 RNAi. These results indicated that DAF-16 is at least partially required for the anti-AD effect of DXN. In conclusion, DXN improved Aß-induced pathological characteristics partially through DAF-2/DAF-16 insulin like pathway in transgenic worms. Together with our data obtained by Morris water maze test, the results showed that DXN markedly ameliorated cognitive performance impairment induced by scopolamine in mice. All the results support that DXN is a potential drug candidate to treat Alzheimer's diseases.

Rose Essential Oil Delayed Alzheimer's Disease-Like Symptoms by SKN-1 Pathway in C. elegans.

There are no effective medications for delaying the progress of Alzheimer's disease (AD), the most common neurodegenerative disease in the world. In this study, our results with C. elegans showed that rose essential oil (REO) significantly inhibited AD-like symptoms of worm paralysis and hypersensivity to exogenous 5-HT in a dose-dependent manner. Its main components of ß-citronellol and geraniol acted less effectively than the oil itself. REO significantly suppressed Aß deposits and reduced the Aß oligomers to alleviate the toxicity induced by Aß overexpression. Additionally, the inhibitory effects of REO on worm paralysis phenotype were abrogated only after skn-1 RNAi but not daf-16 and hsf-1 RNAi. REO markedly activated the expression of gst-4 gene, which further supported SKN-1 signaling pathway was involved in the therapeutic effect of REO on AD C. elegans. Our results provided direct evidence on REO for treating AD on an organism level and relative theoretical foundation for reshaping medicinal products of REO in the future.