Druggability is crucial in pharmaceutical drug development as the source of drug research. Druggability research will face greater challenges because Chinese materia medica (CMM) is the multicomponent drug. In this paper, ideas and methods of study on CMM druggability were mainly proposed in combination with the chemical material basis of muticomponents of CMM.

Objective To evaluate the harmful effects of olanzapine and quetiapine therapeusis on swallowing ability in patients with Alzheimer'disease (AD).Methods AD inpatients with behavioral and psychological symptoms were randomly divided into two groups,treated with olanzapine (n=42) or quetiapine (n=38) for 6 weeks.The patients were assessed with Kubota's water swallowing test and arterial oxygen saturation(SaO2) monitoring pre and pro treatment.Results After treatment,a significant higher score of water swallowing test (t =2.682,2.040;both P＜ 0.05)in either of two groups,and a significant raised degrade of SaO2 only in olanzapine group(t=4.313,P＜0.01)but not in quetiapine group (P＞0.05)were observed.There was a significant higher degrade of SaO2 in olanzapine group than that in quetiapine group (t=2.155,P＜0.05)at 6 weekend of the study.Before pharmacon,about 29％ (23/80) AD subjects were diagnosed as dysphagia.After pharmacon,more emerging dysphagia patients were surveyed in olanzapine group compared with that in quetiapine group(9/31 vs 2/26,x2=4.135,P＜0.05).No significant change (both P＞0.05) in scores of mini-mental state examination(MMSE) and a significant reduced score(t=3.019,2.867;both P＜0.01)of behavioral pathology in Alzheimer'disease rating scale (BEHAVE-AD) were found in both two groups at the end of study.There was no difference among the two groups with regard to score of MMSE or BEHAVE-AD after treatment(both P＞0.05).Conclusion Either olanzapine or quetiapine therapeutics might do some harmful effects on swallowing function in patients with AD,especially the former.

Chronic high-salt diet-associated renal injury is a key risk factor for the development of hypertension. However, the mechanism by which salt triggers kidney damage is poorly understood. Our study investigated how high salt (HS) intake triggers early renal injury by considering the ‘gut-kidney axis’. We fed mice 2% NaCl in drinking water continuously for 8 weeks to induce early renal injury. We found that the ‘quantitative’ and ‘qualitative’ levels of the intestinal microflora were significantly altered after chronic HS feeding, which indicated the occurrence of enteric dysbiosis. In addition, intestinal immunological gene expression was impaired in mice with HS intake. Gut permeability elevation and enteric bacterial translocation into the kidney were detected after chronic HS feeding. Gut bacteria depletion by non-absorbable antibiotic administration restored HS loading-induced gut leakiness, renal injury and systolic blood pressure elevation. The fecal microbiota from mice fed chronic HS could independently cause gut leakiness and renal injury. Our current work provides a novel insight into the mechanism of HS-induced renal injury by investigating the role of the intestine with enteric bacteria and gut permeability and clearly illustrates that chronic HS loading elicited renal injury and dysfunction that was dependent on the intestine.
Animals ; Bacteria ; Bacterial Translocation ; Blood Pressure ; Drinking Water ; Dysbiosis ; Enterobacteriaceae ; Gastrointestinal Microbiome ; Gene Expression ; Hypertension ; Intestines ; Kidney ; Mice* ; Microbiota ; Permeability ; Risk Factors