Since microglia possess both neuroprotective and neurotoxic potential, they play a crucial role in the central nervous system (CNS). Excessive microglial activation induces inflammation-mediated neuronal damage and degeneration. At present, numerous herbal compounds are able to suppress neurotoxicity via inhibiting microglial activation. Therefore, many researchers focus on pharmacological inhibitors of microglial activation to ameliorate neurodegenerative disorders. Further work should concentrate on the exploration of new herbal compounds, which characteristically inhibit microglial neurotoxicity, rather than modulating neuroprotection alone. In this review, we summarize these herbal compounds, which in the past several years have been shown to exert potential neuroprotective activity by inhibiting microglial activation. The therapeutic targets and pharmacological mechanisms of these compounds have also been discussed.

Bacteriocins are known to be natural preservatives, which are becoming increasingly necessary in many types of food to control the proliferation of pathogenic bacteria. In this study, a novel bacteriocin produced by Lactobacillus plantarum ZJ316, called plantaricin ZJ316, was purified by ammonium sulfate precipitation, gel chromatography, and high-performance liquid chromatography. By mass spectrometry, the molecular mass of plantaricin ZJ316 was determined to be 2,366.06 Da. No homologous sequences were found in databases based on comparisons with the N-terminal amino acid sequencing. The bacteriocin was heat resistant and stable after incubation at pH 2.0 to 10.0. It was sensitive to α-chymotrypsin, trypsin, and proteinase K. Plantaricin ZJ316 had a broad inhibitory activity against gram-negative and gram-positive bacteria, especially Listeria monocytogenes. Our results suggested that this bacteriocin has the potential to inhibit pathogenic bacteria in food products.

A high-performance and durable electroosmotic (EO) pump is developed using electropolymerized PANI:PSS/C electrodes. PANI:PSS was electrochemically synthesized on the carbon fiber paper using cyclic voltametry and characterized by a variety of physicochemical methods including field-emission scanning electron microscopy (FESEM), electron probe microanalyzer (EPMA), Fourier transform infrared spectroscopy (FTIR), and X-ray photoelectron spectroscopy (XPS). There was a linear relationship with a regression coefficient R2 ≥ 0.97 between the applied potential and the peak current (Ipeak), maximum flow rate (Qmax), maximum pressure (Pmax), respectively. The EO pump built with PANI:PSS/C electrodes, with an active area of 1.0 cm2, generated the maximum stall pressure of 122 kPa and the maximum flow rate of 203 ul min-1 at 4 V by using deionized (DI) water as a working fluid. The EO pumps assembled with PANI:PSS/C electrodes showed much better overall performances than those made with the bare carbon paper and exhibited good long-term stability without substantial decay for 5 days of continuous operation even at a high potential of 4 V.

Objectives. Guizhi Fuling Formulation (GZFL), a traditional Chinese medical formulation, consists of Cinnamomi Ramulus, Paeoniae Radix Alba (or Paeoniae Radix Rubra), Moutan Cortex, Persicae Semen, and Poria, with multiple therapeutic functions such as sedation, antitumor activity, anti-inflammation, and neuroprotection. However, its clinical applications remain relatively fragmented, and the underlying mechanisms of GZFL in different diseases are still not very certain. Further research and summary in both application and mechanisms remain to be needed for human health and the best use of GZFL. Therefore, we summarized the multiple pharmacologic effects and possible mechanisms of action of GZFL according to recent 17 years of research. Methods. We retrieved four English and two Chinese databases using these keywords (the formulation name or its synonyms) and searched articles written in English from January 2006 up to February 2022. Key Findings. GZFL exhibits multiple pharmacologic advantages in gynecologic diseases and other expanding diseases such as cancer, blood, and vascular disease, renal failure, inflammation, and brain injury. Possibly due to its diverse bioactive components and pharmacologic activities, GZFL could target the multiple signaling pathways involved in regulating blood circulation, inflammatory and immune factors, proliferation, apoptosis, and so on. Conclusion. This review suggests that GZFL displays promising therapeutic effects for many kinds of diseases, which have been beyond the scope of the original prescription for gynecologic diseases. In this way, we wish to provide a reference and recommendation for further preclinic and clinic studies.

Chronic neuroinflammation has been regarded as an important part of the pathological initiation of Alzheimer’s disease (AD), which is associated with the regulation of microglial activation. Preventing microglial activation to inhibit neuroinflammation may become a potential target for the treatment of neurodegenerative diseases. Guizhi Fuling capsule (GZFL) has a strong repression on inflammatory responses. Here, the presenilin1/2 conditional double knockout (PS cDKO) mice, a well-established mouse model of AD, were divided into: WT mice (WT), WT mice+GZFL (WT+GZFL), PS cDKO mice (cDKO), and PS cDKO mice+GZFL (cDKO+GZFL). Mice in the WT+GZFL and cDKO+GZFL group were fed standard chow containing 2000 ppm GZFL for 90 days. After 60 days of GZFL treatment, mice were given to behavioral tests for 30 days in order to explore the effects of GZFL on cognitive and motor function. Then, mice were sacrificed for examining the effects of GZFL on inflammation. Furthermore, primary microglia were obtained from neonatal Sprague-Dawley rats and pretreated with or without GZFL (50 μg/ml) for 1 h in the absence or presence of lipopolysaccharide (LPS) (100 ng/ml) stimulation to speculate whether the underlying mechanism of GZFL’s anti-inflammatory potential was closely associated with Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) signaling pathway. Our findings indicated that GZFL has the ability to alleviate memory deficits in PS cDKO mice, which attributes to the improvement of neuroinflammation by inhibiting microglial activation and the levels of pro-inflammatory mediators. In addition, GZFL could inverse the tau hyperphosphorylation and the lessened expression of synaptic proteins in hippocampus of PS cDKO mice. Furthermore, GZFL prevented LPS-induced neuroinflammatory responses in primary microglia by decreasing the levels of pro-inflammatory mediators. It is noteworthy that therapeutic effects of GZFL on memory impairment are depended on the inhibition of neuroinflammatory responses by the blockage of JAK2/STAT3 signaling pathway. Taken together, GZFL may be an effective compound Chinese medicine for the improvement and postponement of neurodegenerative progression in AD.