本文選題：大黃 + 慢性腎衰竭��； 參考：《南京中醫(yī)藥大學(xué)》2016年博士論文

【摘要】：大黃治療慢性腎衰竭的循證醫(yī)學(xué)證據(jù)目的：評價大黃治療慢性腎衰竭的有效性及安全性。方法：計算機檢索中國生物醫(yī)學(xué)文獻數(shù)據(jù)庫CBM、相關(guān)期刊論文CNKI、維普期刊數(shù)據(jù)庫VIP、萬方資源數(shù)據(jù)庫、EMBASE、MEDLINE、PUBMED、 Cochrane圖書館中關(guān)于大黃治療慢性腎衰竭的隨機和半隨機對照試驗,同時手工檢索相關(guān)期刊雜志,并由兩位研究者進行獨立篩選和資料提取,按照改良Jadad評分量表評價所納入的文獻質(zhì)量,應(yīng)用Revman5.3軟件進行Meta分析。結(jié)果：(一)大黃單方或含大黃的中藥復(fù)方口服治療CRF的系統(tǒng)評價納入35篇文獻,共3060例患者,其中治療組1657例,對照組1403例。Meta分析結(jié)果顯示,與對照組相比,大黃單方或含大黃的中藥復(fù)方口服治療能降低CRF患者Scr[MD=-73.28, 95%CI (-85.96, -60.60) ];降低BUN[MD=-2.47, 95%CI(-3.13, -1.82)];升高CRF患者Ccr[MD=6.66, 95%CI (2.93, 10.40)];升高Hb[MD=9.31, 95%CI (3.81, 14.80)];升高Alb[MD=2.94, 95%CI (1.75, 4.13)];降低24 h尿蛋白定量(24 h UTP) [MD=-0.63, 95%CI (-0.95, -0.30)];降低TG[MD=-0.53, 95%CI (-0.73, -0.32) ]和TC[MD=-1.01, 95%CI (-1.44,-0.58)]；并且可以改善CRF患者癥狀和體征的總有效率[Peto OR=3.42, 95%CI(2.84,4.12)]；但對于減少ESRD的發(fā)生[Peto OR=0.57, 95%CI為(0.19, 1.75)]與對照組相比,差異無統(tǒng)計學(xué)意義。(二)含大黃的中藥灌腸方治療CRF的系統(tǒng)評價納入28篇文獻,共2278例患者,其中治療組1220例,對照組1058例。Meta分析結(jié)果顯示,與對照組相比,含大黃的中藥灌腸方治療能降低CRF患者Scr[MD=-59.62, 95%CI (-88.58, -30.67) ];降低BUN[MD=-3.27, 95%CI (-4.49, -2.05) ];升高CRF患者Ccr[MD=3.95, 95%CI (-0.03, 7.93) ];改善CRF患者癥狀和體征的總有效率[Peto OR=4.08, 95%CI (3.25, 5.12) ];并且可以改善中醫(yī)主要證候納差[MD=-0.48, 95%CI (-0.77, -0.19) ]和惡心嘔吐[MD=- 0.65, 95%CI (- 0.78, - 0.52) ];但對于升高Hb[MD=6.85, 95%CI (-1.82, 15.52) ]、降低尿酸(UA) [MD=-46.84, 95%CI (-102.91, 9.22) ]與對照組相比,差異無統(tǒng)計學(xué)意義。結(jié)論：與對照組相比,大黃單方或含大黃的中藥復(fù)方口服和含大黃的中藥灌腸方均能明顯降低CRF患者Scr、BUN,升高Ccr,同時還能改善患者癥狀和體征的總有效率,大黃單方或含大黃的中藥復(fù)方口服能升高Hb、Alb,降低24h UTP、 TG和TC,但無證據(jù)顯示在減少ESRD的發(fā)生方面較對照組更為有效；另外,含大黃的中藥灌腸方能改善中醫(yī)主要證候納差和惡心嘔吐,但對于升高Hb和降低UA無證據(jù)顯示較對照組更為有效,表明大黃可能是一種相對安全和有效治療CRF的藥物。但由于所納入的文獻存在研究方法學(xué)質(zhì)量低下的問題,因此進一步進行高質(zhì)量文獻研究,對評價其療效及安全性十分必要。大黃素通過自噬途徑對腎小管損傷的保護機制研究背景及目的腎毒性的藥物所致的急性腎功能衰竭早已成為臨床醫(yī)生關(guān)注的重點,順鉑是一種臨床常用于治療多種惡性腫瘤的廣譜、有效的化療藥物,然而,據(jù)統(tǒng)計,臨床上運用順鉑化療后,導(dǎo)致的腎損害發(fā)生率為25%-35%,且順鉑用藥劑量與其引起的腎臟毒性成一定的比例關(guān)系,已成為限制其用量及擴大其應(yīng)用范圍的主要考慮因素。西藥在治療腎毒性藥物所致腎損傷的同時會帶來過多的不良反應(yīng),因此,研究人員致力于尋找一種既能降低順鉑腎毒性,又能保留其抗癌活性的中藥。自噬(autophagy),即溶酶體依賴性的大分子蛋白質(zhì)和細(xì)胞器的自我降解,通過清除衰老的細(xì)胞器和長壽命蛋白質(zhì),為細(xì)胞修復(fù)提供原料與營養(yǎng),實現(xiàn)細(xì)胞器更新。細(xì)胞凋亡,是機體為了保持恒定的細(xì)胞數(shù)目而采取的由基因調(diào)控、生物自主的程序化方式。腎毒性的藥物損傷腎小管主要表現(xiàn)為腎小管上皮細(xì)胞的凋亡,越來越多的實驗研究報道,在順鉑導(dǎo)致的腎臟細(xì)胞凋亡過程中,自噬發(fā)生在凋亡之前,其可能成為其抗凋亡的機制。大黃素是中藥大黃的主要的藥效成分,大量的研究表明其具有保護腎臟的作用,主要集中在抗炎,抑制增殖,抑制細(xì)胞表型轉(zhuǎn)化,以及抗氧化等方面。已有研究報道大黃素能改善順鉑相關(guān)性腎毒性,然而,目前還沒有研究報道大黃素是否可以通過自噬途徑改善順鉑引起的腎損傷。但有研究報道,大黃素是一種有效的單磷酸腺苷(AMP)激活蛋白激酶(AMPK)活化劑,并且可以調(diào)節(jié)哺乳動物的雷帕霉素靶蛋白(mTOR)途徑。由于AMPK/mTOR信號通路在細(xì)胞自噬的調(diào)節(jié)中起著重要的作用,因此,我們推測,在順鉑腎損傷中,大黃素是否有可能通過調(diào)節(jié)自噬而起到腎保護作用。我們選用NRK-52E細(xì)胞作為研究對象,借助順鉑誘導(dǎo)的NRK-52E細(xì)胞損傷模型,通過體外實驗研究,觀察大黃素對順鉑環(huán)境下細(xì)胞自噬相關(guān)蛋白的變化、自噬體形成情況,以及自噬相關(guān)信號通路的影響,進一步探討自噬在腎毒性藥物所致的腎損傷中的變化和大黃素的干預(yù)作用,試圖在體外闡明大黃素通過調(diào)節(jié)自噬相關(guān)信號通路,改善腎毒性藥物所致的腎損傷的分子機制,為大黃素的臨床應(yīng)用提供新的途徑。方法首先,我們觀察了順鉑處理的NRK-52E細(xì)胞形態(tài)和細(xì)胞凋亡相關(guān)的標(biāo)志物表達情況。然后用順鉑加或不加大黃素處理RK-52E細(xì)胞,用顯微進行觀察,并且采用免疫印跡(Western Blot, WB)方法,檢測細(xì)胞凋亡相關(guān)蛋白Caspase-3、cleaved Caspase-3和哺乳動物同源的自噬標(biāo)記蛋白-微管相關(guān)蛋白1輕鏈3(LC3)Ⅰ/Ⅱ表達的情況,以及采用pmRFP-LC3轉(zhuǎn)染技術(shù),利用熒光顯微鏡觀察了大黃素處理細(xì)胞后自噬顆粒在細(xì)胞內(nèi)的表達和分布情況。其次,我們也應(yīng)用自噬體-溶酶體結(jié)合的抑制劑巴弗洛霉素A1,觀察其加入前后對大黃素誘導(dǎo)的自噬的影響。此外,雷帕霉素,哺乳動物的雷帕霉素mTOR靶蛋白的抑制劑,在應(yīng)激條件下可以通過抑制mTOR活性而激活自噬,我們利用免疫印跡,顯微鏡觀察和流式細(xì)胞儀檢測等方法觀察了順鉑和雷帕霉素處理的細(xì)胞形態(tài)變化和細(xì)胞凋亡情況。再次,進一步觀察了大黃素通過調(diào)節(jié)AMPK/mTOR信號通路對自噬活化的影響。采用WB的方法檢測了大黃素處理細(xì)胞后AMPK/mTOF信號通路相關(guān)蛋白的表達情況,與此同時,我們也在大黃素處理的細(xì)胞中加或不加compound C,個公認(rèn)的AMPK印制劑,觀察NRK-52E細(xì)胞形態(tài)和凋亡相關(guān)蛋白的表達。最后,除了上述通路的研究外,我們還觀察了MAPKs家族,包括ERK、P38和JNK所介導(dǎo)的信號通路,是否也參與了大黃素誘導(dǎo)的自噬活化。采用WB方法,檢測了大黃素不同時間點處理細(xì)胞后p-ERK、p-P38和p-JNK蛋白的表達情況,以及LC3-I和LC3-II的表達情況。同時,我們還分別選用了ERK和p38的抑制劑PD098059和SB203580,用大黃素加或不加PD098059和SB203580處理細(xì)胞,觀察p-ERK蛋白、p-p38蛋白的表達情況。結(jié)果(1)隨著順鉑用藥時間和劑量的增加,觀察到細(xì)胞出現(xiàn)凋亡,WB結(jié)果顯示,早期自噬標(biāo)志性蛋白LC3-I幣LC3-Ⅱ的表達增加,LC3-Ⅱ/LC3-Ⅰ的比值增加,晚期凋亡相關(guān)蛋白cleaved Caspase-3的表達增加,CCK-8法和流式細(xì)胞儀檢測結(jié)果與WB的結(jié)果一致,晚期凋亡增加。(2)順鉑處理組存活細(xì)胞數(shù)目減少,經(jīng)大黃素干預(yù)后,存活細(xì)胞數(shù)目明顯增多。免疫印跡處理后,表明大黃素與順鉑共同處理細(xì)胞,能夠明顯逆轉(zhuǎn)單獨順鉑處理細(xì)胞所致的cleaved Caspase-3蛋白的上調(diào)。同時,大黃素處理細(xì)胞,能夠明顯增加LC3-Ⅱ/Ⅰ的比值和自噬顆粒RFP-LC3點狀結(jié)構(gòu)的表達。我們選用雷帕霉素處理細(xì)胞,同樣觀察到其可以增加LC3-I和LC3-Ⅱ的表達,增加]LC3-Ⅱ/LC3-Ⅰ的比值,倒置顯微鏡下觀察到在順鉑和大黃素共同處理細(xì)胞時加入巴佛洛霉素A1,凋亡細(xì)胞數(shù)反而明顯增加。此外,大黃素還能以時間依賴性的方式下調(diào)p-p70S6K蛋白和p-mTOR蛋白的表達,同時上調(diào)p-AMPK蛋白的表達。WB結(jié)果表明,AMPK的抑制齊compoundC能夠明顯的抑制大黃素誘導(dǎo)的MPK的磷酸化,LC3-I向LC3-Ⅱ的轉(zhuǎn)化也被明顯的抑制,熒光顯微鏡觀察的結(jié)果與WB結(jié)果相同,加入了compound C之后,大黃素誘導(dǎo)的紅色熒光自噬顆粒明顯減少。倒置顯微鏡下觀察也發(fā)現(xiàn)compound C能明顯的抑制大黃素的抗凋亡作用,WB結(jié)果同樣表明,大黃素能明顯下調(diào)順鉑誘導(dǎo)的cleaved Caspase-3蛋白的表達,但當(dāng)加入compound C共處理之后,又上調(diào)了cleaved Caspase-3蛋白的表達。(3)WB處理結(jié)果表明,大黃素處理細(xì)胞,p-ERK、p-P38和p-JNK蛋白的表達水平隨著時間的變化先增加后降低；當(dāng)加入ERK的抑制劑PD098059和p38的抑制劑SB203580后,大黃素引起的p-ERK蛋白、p-p38蛋白的增加被抑制。結(jié)論我們的研究結(jié)果發(fā)現(xiàn)順鉑處理NRK-52E細(xì)胞早期可以出現(xiàn)自噬,晚期則出現(xiàn)凋亡。大黃素能誘導(dǎo)自噬,進而達到改善順鉑導(dǎo)致的NRK-52E細(xì)胞凋亡的作用。我們的機制研究結(jié)果提示,AMPK/mTOR信號通路和MAPKs家族成員介導(dǎo)的信號通路可能參與了大黃素誘導(dǎo)自噬的過程。“益腎清利、和絡(luò)泄?jié)岱訙p大黃”辨證方延緩慢性腎衰竭進展的臨床療效觀察目的：評價“益腎清利、和絡(luò)泄?jié)岱訙p大黃”辨證方延緩CRF患者腎功能進展的有效性。方法：采用回顧性的研究方法,選擇2013年9月-2015年9月就診于江蘇省中醫(yī)院腎內(nèi)科導(dǎo)師孫偉教授門診,診斷為慢性腎衰竭的51例患者,觀察“益腎清利、和絡(luò)泄?jié)岱訙p大黃”辨證方治療后,臨床癥狀和療效指標(biāo)的變化,總療程為2年,其中每位患者大黃連續(xù)或間斷用藥療程≥1個月。結(jié)果：51例患者經(jīng)“益腎清利、和絡(luò)泄?jié)岱訙p大黃”辨證方治療24個月后,中醫(yī)臨床癥狀積分較初診時相比顯著下降(P0.01)。經(jīng)治療患者的主要療效指標(biāo)Scr、BUN、UA較治療前相比,均有所下降,具有顯著統(tǒng)計學(xué)差異(P0.01)。治療前后相比較,RBC有所上升,具有顯著統(tǒng)計學(xué)差異(P0.01),治療后Hb輕微上升,但無統(tǒng)計學(xué)差異(P0.05)；治療前后的TC比較,具有顯著統(tǒng)計學(xué)差異(P0.01)；治療后TG有輕微下降,但無統(tǒng)計學(xué)差異(P0.05)。結(jié)論：“益腎清利、和絡(luò)泄?jié)岱訙p大黃”辨證方可以明顯減輕患者臨床癥狀,穩(wěn)定并改善患者的腎功能,不同程度降低Scr、BUN、UA、血脂水平,貧血也一定程度上得到了改善,說明該法很大程度上能延緩腎功能進展,改善患者生活質(zhì)量。
[Abstract]:Evidence based evidence-based medicine for Rhubarb for chronic renal failure: To evaluate the effectiveness and safety of Rhubarb for chronic renal failure. Methods: computer retrieval of Chinese biomedical literature database CBM, Chinese journal full text database CNKI, VP journal database VIP, data base of Wanfang resource, EMBASE, MEDLINE, PUBMED, Cochrane Library A randomized and semi randomized controlled trial of Rhubarb for chronic renal failure was conducted by manual retrieval of periodicals in related journals and two researchers were selected for independent screening and data extraction. The quality of the literature was evaluated according to the modified Jadad scale. The Revman5.3 software was used for Meta analysis. Results: (1) rhubarb single or rhubarb The systematic evaluation of oral Chinese medicine for oral treatment of CRF included 35 articles, including 3060 cases, of which 1657 cases were in the treatment group and 1403 cases in the control group showed that, compared with the control group, the oral administration of rhubarb single or rhubarb compound oral Chinese medicine can reduce Scr[MD=-73.28, 95%CI (-85.96, -60.60)) in CRF patients and reduce BUN[MD=-2.47, 95%CI (-3.13). Ccr[MD=6.66, 95%CI (2.93, 10.40)]; elevated Hb[MD=9.31, 95%CI (3.81, 14.80)]; elevated Alb[MD=2.94, 95%CI (1.75, 4.13)]; reduced 24 h proteinuria (24 h UTP). The total effective rate to improve the symptoms and signs of CRF patients was [Peto OR=3.42, 95%CI (2.84,4.12)]; but there was no significant difference between the control group and the control group for the occurrence of [Peto OR=0.57 in the reduction of ESRD, and (0.19, 1.75)]. (two) the system evaluation of the traditional Chinese medicine enema containing Rhubarb in the treatment of CRF was included in 28 literature, of which the treatment group was 1220. In the control group, 1058 cases of.Meta analysis showed that compared with the control group, Chinese medicine enema containing rhubarb could reduce Scr[MD=-59.62, 95%CI (-88.58, -30.67)) and BUN[MD=-3.27, 95%CI (-4.49, -2.05)] and CRF patient Ccr[MD=3.95, 95 (7.93)), and improve the total effective rate of symptoms and signs of patients. R=4.08, 95%CI (3.25, 5.12)]; and can improve the main syndromes of TCM [MD=-0.48, 95%CI (-0.77, -0.19)] and nausea and vomiting [MD=- 0.65, 95%CI (- 0.78, - 0.52)]; but for the increase of Hb[MD=6.85, 95%CI (-1.82, 15.52)], lower uric acid (UA), compared to the control group, there is no statistical difference. Conclusion: compared with the control group, the Chinese medicine compound of rhubarb single or rhubarb containing oral Chinese medicine and Chinese herbal enema containing rhubarb can significantly reduce the Scr, BUN, Ccr, and improve the total effective rate of the symptoms and signs of CRF patients. The oral administration of rhubarb alone or with rhubarb can increase Hb, Alb, 24h UTP, TG and TC, but it is no more. The evidence shows that the reduction of ESRD is more effective than the control group; in addition, the traditional Chinese medicine enema containing rhubarb can improve the main syndromes and nausea and vomiting of traditional Chinese medicine, but it is more effective for raising Hb and reducing UA than in the control group, suggesting that rhubarb may be a safe and effective drug for the treatment of CRF. There is a problem of low quality of research methodology in the literature included, so it is necessary to further study the high quality literature to evaluate its efficacy and safety. The research background of the protection mechanism of renal tubule injury by autophagy and the acute renal failure caused by the drugs for the purpose of renal toxicity have already become a clinician. The focus of attention, cisplatin is a broad spectrum, effective chemotherapeutic drug commonly used in the treatment of various malignant tumors. However, according to the statistics, the incidence of renal damage caused by cisplatin chemotherapy is 25%-35%, and the dosage of cisplatin is proportional to the renal toxicity caused by cisplatin, which has become a restriction of its dosage and enlargement. The main consideration of the scope of application. Western medicine will bring too many adverse reactions to kidney damage caused by nephrotoxic drugs. Therefore, researchers are committed to finding a traditional Chinese medicine that can reduce the renal toxicity of cisplatin and retain its anticancer activity. Autophagy (autophagy), a lysosomal dependent macromolecule protein and organelle Self degradation, by removing aging organelles and long life proteins to provide material and nutrition for cell repair, and to realize organelle renewal. Cell apoptosis is regulated by genes to maintain a constant number of cells and is bioautonomic programming. Nephrotoxic drug damage renal tubules are mainly shown on renal tubules. A growing number of experimental studies have reported that in the process of renal cell apoptosis induced by cisplatin, autophagy occurs before apoptosis, and it may become a mechanism for its anti apoptosis. Emodin is the main pharmacological component of rhubarb. A large number of studies have shown that it has the role of protecting the kidney, mainly focusing on anti-inflammatory and inhibiting proliferation. It has been reported that emodin can improve cisplatin induced renal damage. However, emodin is an effective monophosphate (AMP) activation protein stimulated by emodin, however, however, it is not reported that emodin can improve cisplatin induced renal damage. Enzyme (AMPK) activator and can regulate the mammalian rapamycin target protein (mTOR) pathway. As the AMPK/mTOR signaling pathway plays an important role in the regulation of autophagy, we speculate whether emodin may play a role in renal protection by autophagy in cisplatin. We choose NRK-52E cells as a cell. With the aid of cisplatin induced NRK-52E cell damage model, the changes in autophagy related proteins, the formation of autophagic bodies and the influence of autophagy related signaling pathways in cisplatin were investigated by cisplatin induced damage model in vitro. The changes of autophagy in renal injury induced by nephrotoxic drugs and emodin were further explored. The effect of the intervention is to elucidate in vitro the molecular mechanism of emodin by regulating autophagy related signaling pathways and improving renal injury induced by nephrotoxic drugs, providing a new approach for the clinical application of emodin. First, we observed the expression of NRK-52E cell morphology and apoptosis related markers in cisplatin treatment. RK-52E cells were treated with cisplatin plus or without enlarging flavin, and the expression of apoptosis related protein Caspase-3, cleaved Caspase-3 and autophagy related protein microtubule related protein 1 light chain 3 (LC3) I / II were detected by Western Blot (WB). The expression and distribution of autophagic particles in cells were observed by fluorescence microscopy. Secondly, we also applied the inhibitor of autophagosome - lysosome binding inhibitor, buffalamycin A1, to observe the effect of emodin on autophagy induced by emodin. In addition, rapamycin, rapamycin mTOR in mammals The inhibitor of target protein can activate autophagy by inhibiting the activity of mTOR under stress conditions. We observed the morphological changes and apoptosis of cisplatin and rapamycin by immunoblotting, microscope observation and flow cytometry. Again, the emodin was observed by adjusting the AMPK/mTOR signal. The effect of pathway on autophagy activation. WB method was used to detect the expression of AMPK/mTOF signaling pathway related proteins after emodin treated cells. At the same time, we also added or without compound C in emodin treated cells, a recognized AMPK printing agent, to observe the expression of NRK-52E cell morphology and apoptosis related proteins. Finally, the expression of apoptosis related proteins was observed. In addition to the above pathway, we also observed whether the MAPKs family, including ERK, P38 and JNK, also participated in emodin induced autophagy activation. The expression of p-ERK, p-P38 and p-JNK protein, as well as the expression of LC3-I and LC3-II, were detected by the WB method. We also selected ERK and p38 inhibitors PD098059 and SB203580 respectively. The expression of p-ERK protein and p-p38 protein was observed with emodin plus or without PD098059 and SB203580 cells. Results (1) the apoptosis of cells was observed with the increase of time and dosage of cisplatin. WB results showed that the early autophagic marker protein LC3-I currency LC3 was found. The expression of - II increased, the ratio of LC3- II /LC3- I increased, and the expression of advanced apoptosis related protein cleaved Caspase-3 increased. The results of CCK-8 and flow cytometry were consistent with the results of WB, and advanced apoptosis increased. (2) the number of surviving cells in cisplatin treatment group decreased, and the number of surviving cells increased significantly after the prognosis of emodin. Immunoblotting The results showed that the CO treatment of emodin and cisplatin could obviously reverse the up regulation of cleaved Caspase-3 protein caused by cisplatin treated cells. At the same time, emodin treated cells could significantly increase the ratio of LC3- II / I and the expression of RFP-LC3 dot structure of autophagy particles. It could increase the expression of LC3-I and LC3- II and increase the ratio of]LC3- II /LC3- I. Under the inverted microscope, it was observed that the number of apoptotic cells increased obviously when cisplatin and emodin co treated cells, and the number of apoptotic cells increased significantly. In addition, emodin could also reduce the expression of p-p70S6K and p-mTOR protein in a time dependent manner. The expression of p-AMPK protein expression.WB showed that AMPK inhibition of homogeneous compoundC could obviously inhibit the phosphorylation of MPK induced by emodin, and the transformation of LC3-I to LC3- II was obviously suppressed. The results of fluorescence microscopy were the same as WB. After adding compound C, the red fluorescent autophagic particles induced by emodin was significantly reduced. Compound C could obviously inhibit the anti apoptotic effect of emodin. WB results also showed that rhubarb could obviously reduce the expression of cleaved Caspase-3 protein induced by cisplatin, but when compound C was added, the expression of cleaved Caspase-3 protein was up-regulated. (3) the result of WB treatment showed emodin. The expression level of p-ERK, p-P38 and p-JNK protein increased first and then decreased with the change of time; the increase of p-ERK protein and p-p38 protein caused by emodin was inhibited when the inhibitor of ERK was added to PD098059 and p38, the inhibitor of SB2035 80. Conclusion our results showed that autophagy could occur at the early stage of cisplatin treatment for NRK-52E cells. There is apoptosis in late stage. Rhein can induce autophagy to improve the apoptosis of NRK-52E cells induced by cisplatin. Our mechanism study suggests that the signal pathway mediated by AMPK/mTOR signaling pathway and MAPKs family members may be involved in the process of emodin induced autophagy. The clinical effect of syndrome differentiation in delaying the progress of chronic renal failure: To evaluate the effectiveness of "Yishen Qingli, harmony and turbidity method plus subtraction of rhubarb" to delay the progression of renal function in CRF patients. Methods: a retrospective study was adopted to select professor Sun Wei's clinic in Jiangsu Province Traditional Chinese Medicine Hospital, the nephrology department of Jiangsu Province Traditional Chinese Medicine Hospital in September September 2013. 51 cases of chronic renal failure were diagnosed and observed the changes of clinical symptoms and curative effects for 2 years after the treatment of "Yishen Qingli, rhubarb and rhubarb", and the course of treatment for each patient was more than 1 months. Results: 51 patients were identified by "Yishen Qingli, harmony and turbidity method adding rhubarb" After 24 months of treatment, the clinical symptom score of TCM was significantly lower than that of the first diagnosis (P0.01). The main curative effect indexes of the patients were Scr, BUN, UA compared with before treatment, and there were significant differences (P0.01). After treatment, RBC had a significant difference (P0.01), and Hb slightly increased after treatment. But there was no statistical difference (P0.05). There was a significant difference in TC between before and after treatment (P0.01), but there was a slight decrease in TG after treatment.
【學(xué)位授予單位】：南京中醫(yī)藥大學(xué)
【學(xué)位級別】：博士
【學(xué)位授予年份】：2016
【分類號】：R277.5

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