Objective To study the efficacy and safety of oral calcium carbonate suspension and proton pump inhibitors (PPI) in symptoms relief of acid related diseases.Methods The multi-center,randomized and controlled study was carried out.A total of 400 acid-related diseases patients from 14 to 70 years old with at least one of moderate or severe symptoms such as acid regurgitation,epigastric pain,epigastric discomfort,upper abdominal burning or distension were equally divided into two groups and treated with oral calcium carbonate suspension or omeprazole enteric-coated tablets.The onset of symptoms relief of all patients of the first time after taking medicine was observed.The relief of clinical symptoms at the third day and seventh day after taking medicine was also observed.The adverse events were recorded.Analysis of variance was performed for statistical analysis.Results The onset of symptoms relief of oral calcium carbonate suspension group in acid regurgitation,epigastric pain,epigastric discomfort,upper abdominal burning or distension of the first time after taking medicine were significantly faster than those of PPI group (F=4.866,8.142,41.366,6.955,35.252; all P＜0.05).At the third day after taking medicine,the treatment efficiency of oral calcium carbonate suspension group and PPI group were 69.50％ and 72.50％,and at the seventh day the treatment efficiency of oral calcium carbonate suspension group and PPI group were 92.00％ and 96.50％.There was no significant difference in treatment efficiency and comprehensive efficacy between two groups at day three and seven after taking medicine (both P＞ 0.05).There were 14 cases of mild adverse events and two cases of moderate adverse events in oral calcium carbonate suspension group.There were 10 cases of mild adverse events in PPI group.There was no significant difference between two groups (P＞0.05).Conclusion Oral calcium carbonate suspension provides faster symptom relief than PPI and can effectively improve the symptoms of acid-related diseases.

Objective:To explore the effect and mechanism of taxifolin (TAX) on ameliorating cisplatin-induced renal oxidative damage.Methods:(1) Forty male C57BL/6 mice were divided into 4 groups: control group ( n=10), TAX group ( n=10), cisplatin group ( n=10) and cisplatin+TAX group ( n=10). The weight of mice in each group was measured. The level of serum creatinine (Scr) and blood urea nitrogen (BUN) was analyzed. Kidney histopathological change in mice was analyzed by HE staining. The pro-inflammatory cytokines levels of interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-α) were measured by enzyme linked immunosorbent assay. The levels of reactive oxygen species (ROS), malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT) and glutathione (GSH) were measured by multifunctional microplate reader. The expression of inflammatory factors, antioxidant genes, and peroxisome proliferator-activated receptor γ coactivator-1α ( PGC- 1) mRNA were measured by real-time PCR. Evaluation of mitochondrial function by measuring ATP level and mtDNA content. Determination of AMP-activated protein kinase (AMPK) and phosphorylated AMPK protein expression by Western blotting. (2) Evaluate the effect of taxifolin on chemotherapy of cisplatin by establishing Lewis lung cancer transplantation tumor C57BL/6 mice model. Results:Compared with the control group, the weight of the mice in the TAX group was not significantly reduced ( P>0.05), and there was no obvious kidney damage ( P>0.05), indicating that oral TAX had good safety. Compared with the cisplatin group, TAX could significantly delay cisplatin-induced the weight loss of mice, reduce the levels of Scr and BUN, and alleviate the pathological changes of kidney tissue (all P<0.05). TAX could reduce the levels of serum inflammatory factors IL-6 and TNF-α and the expression of renal inflammatory factors IL- 6, TNF- α and IL- 1β mRNA induced by cisplatin in mice (all P<0.05). TAX could significantly reduce the levels of ROS and MDA, and increase the activities of SOD, CAT and GSH in cisplatin-induced acute kidney injury mice (all P<0.01). Meanwhile, TAX could up-regulate the mRNA expression of UCP2, SOD2, CAT antioxidant genes and PGC- 1α in the kidneys of mice with acute kidney injury induced by cisplatin, and increase the levels of ATP and mtDNA in cisplatin-induced acute kidney injury mice (all P<0.01). Western blotting results showed that TAX significantly promoted the expression of phosphorylated AMPK protein in cisplatin-induced acute kidney injury mice ( P<0.01). In addition, through the establishment of Lewis lung cancer transplantation tumor C57BL/6 mice model, it was found that TAX had no significant effect on the anti-tumor efficacy of cisplatin. Conclusions:TAX can ameliorate cisplatin-induced renal oxidative damage, and its mechanism may be related to the activation of AMPK/PGC-1α pathway.