Antibiotic resistance is becoming significantly prominent and urgent in clinical practice with the increasing and wide application of antibacterial drugs. However, developing and synthesizing new antimicrobial drugs is costly and time-consuming. Recently, researchers shifted their sights to traditional Chinese medicine (TCM). Here, we summarized the inhibitory mechanism of TCM herbs and their active ingredients on bacteria, discussed the regulatory mechanism of TCM on antibiotic-resistant bacteria, and revealed preclinical results of TCM herbs and their active components against antibiotic-resistant bacteria in mouse models. Those data suggest that TCM herbs and their effective constituents exhibit potential blockage ability on antibiotic-resistant bacteria, providing novel therapeutic ideas for reversing antibiotic resistance.

BackgroundIschemic stroke often induces profound white matter lesions, resulting in poor neurological outcomes and impaired post-stroke recovery. The present study aimed to investigate the effects of cornel iridoid glycoside (CIG), a major active component extracted from Cornus officinalis, on the white matter injury induced by ischemic stroke and further investigate its neuroprotective mechanisms.MethodsAdult male Sprague-Dawley rats underwent middle cerebral artery occlusion (MCAO) surgery for 2 h, followed by reperfusion. Rats were intragastrically administered CIG (60 mg/kg and 120 mg/kg) beginning 6 h afters reperfusion, once daily for seven days. A series of behavioral tests (modified neurological severity scores test, object recognition test, adhesive removal test, and beam walking test) were performed to evaluate the neurological functioning in MCAO rats. Histology of the white matter was studied using luxol fast blue staining and transmission electron microscopy. Immunohistochemical staining was performed to assess myelin loss, oligodendrocyte maturation, and glial activation. Activation of the brain-derived neurotrophic factor (BDNF)/neuregulin-1 (NRG1) pathway was evaluated by Western blotting.ResultsCIG treatment remarkably decreased the neurological deficit score, accelerated the recovery of somatosensory and motor functions, and ameliorated the memory deficit in MCAO rats. Furthermore, CIG alleviated white matter lesions and demyelination, increased myelin basic protein expression and the number of mature oligodendrocytes, and decreased the number of activated microglia and astrocytes in the corpus callosum of MCAO rats. In addition, Western blot analysis indicated that CIG increased the expression of BDNF/p-TrkB, NRG1/ErbB4 proteins, which further elevated PI3K p110α/p-Akt/p-mTOR signaling in the corpus callosum of MCAO rats.ConclusionWe demonstrated that CIG protects against white matter lesions induced by cerebral ischemia partially by decreasing the number of activated microglia and astrocytes, increasing BDNF level, and activating NRG1/ErbB4 and its downstream PI3K/Akt/mTOR pathways in the white matter. CIG might be used as a potential neuroprotective agent for the treatment of ischemic stroke.

Hydroxyproline O-arabinosylation is a highly-conserved and plant-specific post-translational modification found on extensins and other structural proteins in the cell wall, and is catalyzed by Hydroxyproline O-arabinosyltransferases (HPATs). In Arabidopsis, loss of HPAT1 and HPAT3 (hpat1/3) causes reorganization of components in the pollen tube (PT) cell wall, which compromises cell wall structural integrity and decreases PT growth and fertility. We have previously shown that reduced secretion (caused by loss-of-function mutations in secretory genes EXO70A2, SEC15A, and SEC1A) suppressed cell wall defects and strongly rescued poor growth and fertility in hpat1/3 PTs. Here, we show that a missense mutation in PHOSPHOLIPASE C6 (PLC6) also rescues hpat1/3 PT growth and fertility. Transgenic insertion mutations that disrupt PLC6 expression did not improve hpat1/3 pollen fertility, and did not affect PT growth or fertility in the wild type background. This data suggests that our missense allele (plc6-4) does not function like a true loss-of-function allele, and that PLC6 is not required for wild type PT growth. However, in the absence of hpat1/3, plc6-4 PTs have defects in transmission and polarized growth, as indicated by meandering growth paths and a resulting crooked appearance. plc6-4 PT elongation and straightness are more sensitive to elevated levels of calcium than wild type. This may be due the nature of the plc6-4 mutation, which causes an E569K amino acid substitution in the lipid-binding C2 domain. The 569 position is located among conserved residues that bind calcium. The resulting charge inversion caused by the E569K substitution may disrupt the lipid binding and phospholipase activities of PLC6. Here, we show that PLC6 influences polarized PT growth and HPAT-mediated PT growth and fertility, and future studies are necessary to better understand the relationship between calcium and PLC6 in PT growth.