Oligodendrocyte (OL) myelination is a critical process for the neuronal axon function in the central nervous system. After demyelination occurs because of pathophysiology, remyelination makes repairs similar to myelination. Proliferation and differentiation are the two main stages in OL myelination, and most factors commonly play converse roles in these two stages, except for a few factors and signaling pathways, such as OLIG2 (Oligodendrocyte transcription factor 2). Moreover, some OL maturation gene mutations induce hypomyelination or hypermyelination without an obvious function in proliferation and differentiation. Herein, three types of factors regulating myelination are reviewed in sequence.

The C-O homolytic bond dissociation enthalpies(BDEs) were calculated by high-level ab initio including G4, G3B3, G3, CBS-QB3 and a series of density function theory (DFT) methods. It is found that the wB97 method gave the most reliable C-O BDEs and the root-mean-square deviation (RMSD) is 7.6 kJ/mol. Therefore, the C(sp(2))-O BDE predictions and the substituent effects of alkenyl phosphates/sulfonates and aryl phosphates/sulfonates were investigated in detail by using the wB97 method. Interestingly, there exist different substituent effects in α- and β-substituted alkenyl phosphates/sulfonates. Excellent linear relationships between the C-O BDEs of β-substituted alkenyl phosphates/sulfonates with substituent constant σp(+) were found. In addition, the NBO analysis further disclosed the essence of the substituent effects on C-O BDEs.

The alkenyl/aryl C(sp2)–O cleavage and the substituent effect in both carboxylates/carbamates and corresponding Ni complexes were investigated in detail by wB97 method.

The present study aimed to characterize the glucan from C. mollissima Blume fruits and its selenium derivative, then investigate their antitumor activity in vitro. A glucan, designated as CPA, was firstly isolated from the fruits of C. mollissima Blume. Structure analysis indicated that CPA was a linear 1,6-α-D-glucan with the average molecular weight about 2.0 × 10 kDa. The selenylation modification derivative of CPA (sCPA), exhibited a stronger antiproliferative effect on tumor cells than CPA in vitro. CPA and sCPA could induce HeLa cells apoptosis and decrease mitochondrial membrane potential. sCPA could also arrest HeLa cells in S phase, promote reactive oxygen species generation and activate caspase-3 activity in HeLa cells. These results manifest that CPA and sCPA inhibit the proliferation of HeLa cells via different mechanisms, which is meaningful for their potential use as antitumor drugs.

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