Effect of Sheng-jiang powder on multiple-organ inflammatory injury in acute pancreatitis in rats fed a high-fat diet

BACKGROUND Obesity worsens inflammatory organ injury in acute pancreatitis(AP), but there is no effective preventive strategy. Sheng-jiang powder(SJP) has been shown to alleviate multiple-organ inflammatory injury in rats with high-fat diet-induced obesity. Hence, SJP is supposed to have an effect on multiple-organ inflammatory injury in AP in rats fed a high-fat diet.AIM To explore how obesity may contribute to aggravating inflammatory organ injury in AP in rats and observe the effect of SJP on multiple-organ inflammatory injury in AP in rats fed a high-fat diet.METHODS Rats were randomly assigned to a control group(CG), an obese group(OG), and an SJP treatment group(SG), with eight rats per group. The rats in the OG and SG were fed a high-fat diet. From the third week, the rats in the SG were given oral doses of SJP(5 g/kg of body weight). After 12 wk, AP was induced in the three groups. Serum amylase level, body weight, Lee's index, serum biochemistry parameters, and serum inflammatory cytokine and tissue cytokine levels were assessed, and the tissue histopathological scores were evaluated and compared.RESULTS Compared with the CG, serum triglyceride, total cholesterol, interleukin-6, and interleukin-10 levels were significantly higher in the OG, and serum high-density lipoprotein cholesterol level was significantly lower in the OG. Moreover,enhanced oxidative damage was observed in the pancreas, heart, spleen, lung,intestine, liver, and kidney. Evidence of an imbalanced antioxidant defense system, especially in the pancreas, spleen, and intestine, was observed in the obese AP rats. Compared with the OG, serum high-density lipoprotein cholesterol, interleukin-10, and superoxide dismutase expression levels in the pancreas, spleen, and intestine were increased in the SG. Additionally, SJP intervention led to a decrease in the following parameters: body weight; Lee's index; serum triglyceride levels; serum total cholesterol levels; malondialdehyde expression levels in the pancreas, heart, spleen, lung, and liver; myeloperoxidase expression levels in the lung; and pathological scores in the liver.CONCLUSION Obesity may aggravate the inflammatory reaction and pathological multipleorgan injury in AP rats, and SJP may alleviate multiple-organ inflammatory injury in AP in rats fed a high-fat diet.

Sheng-jiang powder ameliorates obesity-induced pancreatic inflammatory injury via stimulating activation of the AMPK signalling pathway in rats

AIM To investigate the mechanisms by which Sheng-jiang powder(SJP) ameliorates obesity-induced pancreatic inflammatory injury.METHODS Sprague-Dawley rats were randomized into three groups: normal group(NG), obese group(HLG), or SJP treatment group(HSG). Obesity was induced by feeding a high-fat diet in the HLG and HSG, while the NG received standard chow. Rats were euthanized after 12 wk, and blood and pancreatic tissues were collected for histopathological analyses. Nuclear factor kappa-light-chain-enhancer of activated B cells(NF-κB) and transforming growth factor beta(TGF-β) expression, serum triglyceride and adiponectin levels, and apoptosis in pancreatic acinar cells were assessed. A high-fat AR42 J acinar cell injury model was established using very low-density lipoprotein(VLDL). AR42 J acinar cell culture supernatant, treated with different interventions, was applied to seven groups of pancreatic stellate cells(PSCs). The proliferation of PSCs and the expression of fibronectin and type I collagenase were assessed.RESULTS Compared with the NG, we found higher pathological scores for pancreatic tissues, lower serum adiponectin levels, higher expression levels of NF-κB in pancreatic tissues and TGF-β in pancreatic inflammatory cells, and increased apoptosis among pancreatic acinar cells for the HLG(P < 0.05). Compared with the HLG, we found reduced body weight, Lee's index scores, serum triglyceride levels, and pathological scores for pancreatic tissues; higher serum adiponectin levels; and lower expression levels of NF-κB, in pancreatic tissue and TGF-β in pancreatic inflammatory cells for the HSG(P < 0.05). The in vitro studies showed enhanced PSC activation and increased expression levels of fibronectin and type I collagenase after SJP treatment. An adenosine 5‘-monophosphate-activated protein kinase(AMPK) inhibitor inhibited PSC activation.CONCLUSION SJP may ameliorate obesity-induced pancreatic inflammatory injury in rats by regulating key molecules of the adiponectin-AMPK signalling pathway.

甘露消毒丹合升降散治疗小儿急性化脓性扁桃体炎100例临床观察

目的:观察甘露消毒丹合升降散加减治疗急性化脓性扁桃体炎的临床疗效及其安全性。方法:选取200例急性化脓性扁桃体炎患儿,随机分成观察组和对照组。对照组口服阿莫西林克拉维酸钾片;观察组使用甘露消毒丹合升降散加减。两组均持续治疗5 d,比较两组患儿的临床症状、体征改善情况、疗效及不良反应情况。结果:观察组总有效率及临床治愈率分别是98%、78%,对照组总有效率及临床治愈率分别是88%、58%,经Wilcoxon秩和检验比较,两组疗效差异具有统计学意义(P<0.05);两组在体温恢复正常时间、咽痛完全缓解时间、扁桃体脓点消失时间、扁桃体肿大或充血消退时间方面比较,观察组均比对照组时间缩短,差异有统计学意义(P<0.05)。结论:甘露消毒丹合升降散加减能迅速改善小儿急性化脓性扁桃体炎临床表现,可推广应用。

升降散治疗内伤发热例析

内伤发热是指以内伤为病因,脏腑功能失调,气血阴阳失衡为基本病机所致的发热,往往起病缓慢,病程较长。李小娟教授根据临床经验采用中医辨证治疗,疗效甚佳。

赵进喜教授应用升降散治疗肾脏病理论撷英

升降散出自清代名医杨栗山的《伤寒瘟疫条辨》,曾被作为治疗温病的主方。赵进喜教授将“郁热内结、湿浊邪毒阻滞气机”作为本方治疗的关键病机,将发热不退或头痛眩晕、恶心呕吐、心胸烦闷、大便不畅、脉数急作为升降散的临证要点,同时强调辨证与辨病相结合,随证灵活化裁。现将从升降散的病机、方源、适应证、临床应用等方面进行初步讨论。

升降散联合针灸治疗对肥胖相关性肾病患者血清瘦素、脂联素的影响

目的:观察升降散加减方联合针灸治疗对肥胖相关性肾病患者24 h尿微量白蛋白排泄率(Urinary Albumin Excretion Rate UAER)及血清瘦素(leptin)、脂联素(adiponectin)的影响。方法:将50例肥胖相关性肾病患者按随机数字表法分为2组,对照组给予生活方式干预、适当运动、饮食控制、厄贝沙坦口服,治疗组在上述治疗基础上加用自拟升降散加减方配以针灸治疗,比较2组治疗前后UREA、血清瘦素、脂联素的变化。结果:治疗组在降低24 h尿微量白蛋白排泄率、降低血清瘦素及升高脂联素方面均好于治疗前,且明显优于对照组,对照组在降低24 h尿微量白蛋白排泄率、降低血清瘦素、升高脂联素方面不明显。结论:升降散加减方联合针灸治疗可降低肥胖相关性肾病患者UAER和血清瘦素,升高脂联素。

郑启仲运用升降散规律研究

目的:研究郑启仲教授运用升降散用药规律。方法:通过收集郑启仲教授门诊处方,录入中医传承辅助平台,使用软件的统计报表模块、数据分析模块和关联规则apriori算法等数据挖掘方法,分析处方中药物应用频次、药物组合频次等,并进行关联规则分析,重点分析发热和咳嗽为主症的用药规律,研究郑启仲教授运用升降散用药规律。结果:应用关联规则分析发现升降散常与柴胡、黄芩、生石膏、甘草等配伍。发热为主症的疾病常用处方:升降散、普济消毒饮、银翘散等,多与生石膏、栀子、浙贝母、羚羊角等药物配伍。咳嗽为主症的疾病常用处方:升降散、麻杏石甘汤、三拗汤、小柴胡汤等,多与川贝母、莱菔子、连翘、栀子、葶苈子、羚羊角等配伍。结论:郑启仲教授灵活运用升降散治疗儿科外感温病及内伤杂病,擅用升清降浊治法,组方用药体现了升清降浊的治疗思想。