Protective Effect and Mechanism of Placenta Extract on Liver

The placenta contains multiple biologically active substances, which exert antioxidation, anti-inflammatory, immunomodulatory, and delayed aging effects. Its extract can improve hepatic morphology and function: on the one hand, it can reduce liver interstitial collagen deposition, lipogenesis, and inflammatory cell infiltration and improve fibrosis; on the other hand, it can prevent hepatocellular degeneration by scavenging reactive oxygen species (ROS) and inhibiting inflammatory cytokine production, further improve hepatocyte apoptosis and necrosis, and promote hepatocyte regeneration, making it a promising liver-protective agent. Current research on placenta extract (PE) mainly focuses on treating a specific type of liver injury, and there are no systematic reports. Therefore, this review comprehensively summarizes the treatment reports of PE on liver injury and analyzes its mechanism of action.     

儿茶素类化合物对四氯化碳致大鼠慢性肝损伤的保护作用

目的　观察儿茶素类化合物保肝降酶的作用。方法　制备大鼠的四氯化碳 (CCl4)慢性肝损伤模型 ,观察儿茶素类化合物对肝损伤大鼠血清丙氨酸转氨酶 (ALT)、天冬氨酸转氨酶 (AST)、丙二醛 (MDA)等的影响 ,以及肝组织羟脯氨酸含量和肝脏组织结构的变化。结果　儿茶素类化合物给药 2个月后 ,中、高剂量给药组 (10 0 ,2 0 0mg/kg)均能降低血清ALT的活力以及脂质过氧化产物MDA和肝组织羟脯氨酸的含量 (P <0 0 1或P <0 0 5 ) ,其降低肝组织羟脯氨酸含量的作用与联苯双酯相当。肝组织的病理改善情况两药相似 ,而抗膜脂质过氧化作用优于联苯双酯。结论　儿茶素类化合物具有保护化学性肝损伤作用 ,有降低转氨酶活力、减轻肝脏病理损伤的作用     

Alanyl-Glutamine Protects Mice against Methionine- and Choline-Deficient-Diet-Induced Steatohepatitis and Fibrosis by Modulating Oxidative Stress and Inflammation

Nonalcoholic steatohepatitis (NASH) is a common chronic liver disease with increasing prevalence rates over years and is associated with hepatic lipid accumulation, liver injury, oxidative stress, hepatic inflammation, and liver fibrosis and lack of approved pharmacological therapy. Alanyl-glutamine (Ala-Gln) is a recognized gut-trophic nutrient that has multiple pharmacological effects in the prevention of inflammation- and oxidative-stress-associated diseases. Nevertheless, whether Ala-Gln has a protective effect on NASH still lacks evidence. The aim of this study is to explore the influence of Ala-Gln on NASH and its underlying mechanisms. Here, C57BL/6 mice were fed a methionine- and choline-deficient (MCD) diet to establish the model of NASH, and Ala-Gln at doses of 500 and 1500 mg/kg were intraperitoneally administered to mice along with a MCD diet. The results showed that Ala-Gln treatment significantly attenuated MCD-induced hepatic pathological changes, lowered NAFLD activity score, and reduced plasma alanine transaminase (ALT), aspartate transaminase (AST) and lactate dehydrogenase (LDH) levels. Ala-Gln dramatically alleviated lipid accumulation in liver through modulating the expression levels of fatty acid translocase (FAT/CD36) and farnesoid X receptor (FXR). In addition, Ala-Gln exerted an anti-oxidant effect by elevating the activities of superoxide dismutase (SOD) and glutathione peroxidase (GPX). Moreover, Ala-Gln exhibited an anti-inflammatory effect via decreasing the accumulation of activated macrophages and suppressing the production of proinflammatory mediators. Notably, Ala-Gln suppressed the development of liver fibrosis in MCD-diet-fed mice, which may be due to the inhibition of hepatic stellate cells activation. In conclusion, these findings revealed that Ala-Gln prevents the progression of NASH through the modulation of oxidative stress and inflammation and provided the proof that Ala-Gln might be an effective pharmacological agent to treat NASH.     

Shibi Tea (Adinandra nitida) and Camellianin A Alleviate CCl4-Induced Liver Injury in C57BL-6J Mice by Attenuation of Oxidative Stress,Inflammation, and Apoptosis

Liver injury is a significant public health issue nowadays. Shibi tea is a non-Camellia tea prepared from the dried leaves of Adinandra nitida, one of the plants with the greatest flavonoid concentration, with Camellianin A (CA) being the major flavonoid. Shibi tea is extensively used in food and medicine and has been found to provide a variety of health advantages. The benefits of Shibi tea and CA in preventing liver injury have not yet been investigated. The aim of this study was to investigate the hepatoprotective effects of extract of Shibi tea (EST) and CA in mice with carbon tetrachloride (CCl₄)-induced acute liver injury. Two different concentrations of EST and CA were given to model mice by gavage for 3 days. Treatment with two concentrations of EST and CA reduced the CCl₄-induced elevation of the liver index, liver histopathological injury score, alanine aminotransferase (ALT), and aspartate aminotransferase (AST). Western blotting and immunohistochemical analysis demonstrated that EST and CA regulated the oxidative stress signaling pathway protein levels of nuclear factor E2-related factor 2 (Nrf2)/heme-oxygenase-1 (HO-1), the expression of inflammatory cytokines, the phosphorylated nuclear factor-kappaB p65 (p-NF-κB)/nuclear factor-kappaB p65 (NF-κB) ratio, the phospho-p44/42 mitogen-activated protein kinase (p-MAPK), and the apoptosis-related protein levels of BCL2-associated X (Bax)/B cell leukemia/lymphoma 2 (Bcl2) in the liver. Taken together, EST and CA can protect against CCl₄-induced liver injury by exerting antioxidative stress, anti-inflammation, and anti-apoptosis.     

Protective Effects Induced by a Hydroalcoholic Allium sativum Extract in Isolated Mouse Heart

The aim of the present study was to investigate the possible protective effects of a garlic hydroalcoholic extract on the burden of oxidative stress and inflammation occurring on mouse heart specimens exposed to E. coli lipopolysaccharide (LPS), which is a well-established inflammatory stimulus. Headspace solid-phase microextraction combined with the gas chromatography–mass spectrometry (HS-SPME/GC–MS) technique was applied to determine the volatile fraction of the garlic powder, and the HS-SPME conditions were optimized for each of the most representative classes of compounds. CIEL*a*b* colorimetric analyses were performed on the powder sample at the time of delivery, after four and after eight months of storage at room temperature in the dark, to evaluate the color changing. Freshly prepared hydroalcoholic extract was also evaluated in its color character. Furthermore, the hydroalcoholic extract was analyzed through GC–MS. The extract was found to be able to significantly inhibit LPS-induced prostaglandin (PG) E₂ and 8-iso-PGF_2α levels, as well as mRNA levels of cyclooxygenase (COX)-2, interleukin (IL)-6, and nuclear factor-kB (NF-kB), in heart specimens. Concluding, our findings showed that the garlic hydroalcoholic extract exhibited cardioprotective effects on multiple inflammatory and oxidative stress pathways.     

四种食用真菌提取物预防小鼠酒精性氧化损伤的研究

[目的 ]评价灵芝、云芝、灰树花、姬松茸 4种食用真菌提取物预防小鼠酒精性氧化损伤的作用。 [方法 ]每日灌服 4种食用真菌提取物 ,每鼠各 1 5g/kgbw ,共 3 0d ,结束时阳性对照组及各受试物组一次灌胃 5 0 %乙醇 12ml/kg ,阴性对照组给予 70 %葡萄糖溶液 ,禁食 12h后处死。检测血清谷丙转氨酶 (ALT)、谷草转氨酶 (AST)和谷胱甘肽s 转移酶 (GST)、肝匀浆丙二醛 (MDA)、还原型谷胱甘肽 (GSH)、谷胱甘肽过氧化物酶 (GSH Px)、超氧化物歧化酶 (SOD)和甘油三酯 (TG)。同时计算肝体比。 [结果 ]灵芝提取物组GSH、GSH Px显著升高 (P <0 0 5 ) ,MDA、TG含量明显下降 (P <0 0 5 )。[结论 ]给予小鼠相同剂量的 4种真菌提取物 ,其中灵芝提取物有较好的预防酒精性氧化损伤作用     

Protective Effects of Spirulina maxima against Blue Light-Induced Retinal Damages in A2E-Laden ARPE-19 Cells and Balb/c Mice

Age-related macular degeneration (AMD) is a significant visual impairment in older people, and there is no treatment for dry AMD. Spirulina maxima (S. maxima), a cyanobacterium, has inhibitory effects against oxidative stress. However, the protective effects of S. maxima and its underlying mechanisms on blue light (BL)-caused macular degeneration are unknown. We aimed to investigate the protective effects of S. maxima on blue light-caused retinal damage and demonstrate its underlying mechanisms in human retinal pigment epithelial (ARPE-19) cells and Balb/c retinas. Additionally, the active component of S. maxima was examined in the RPE cells. In vitro, S. maxima decreased BL-induced RPE cell death by inhibiting reactive oxygen species (ROS) production. S. maxima inhibited BL-induced inflammation via regulating the NF-κB pathway, inflammatory-related gene expression, and the apoptosis pathway in RPE cells. In vivo, administration of S. maxima inhibited BL-induced retinal degeneration by restoring the thicknesses of whole retina, ONL (outer nuclear layer), INL (inner nuclear layer), and PL (photoreceptor layer) by BL exposure. Phycocyanin exerted protective effects in the pre-and post-treatment system. Therefore, S. maxima could be a potential nutraceutical approach to intercept the patho-physiological processes leading to dry AMD and advancement to wet AMD. Moreover, phycocyanin was a major active compound of S. maxima. These findings need to be investigated in human studies, particularly through a clinical trial.     

Protective Effects of Naringenin from Citrus sinensis (var. Valencia) Peels against CCl4-Induced Hepatic and Renal Injuries in Rats Assessed by Metabolomics,Histological and Biochemical Analyses

Citrus fruits are grown worldwide for their special nutritive and several health benefits. Among citrus bioactives, naringenin, a major flavanone, exhibits a potential hepatoprotective effect that is not fully elucidated. Herein, serum biochemical parameters and histopathological assays were used to estimate the hepatoprotective activity of naringenin, isolated from Citrus sinensis (var. Valencia) peels, in CCl₄-induced injury in a rat model. Further, GC–MS-based untargeted metabolomics was used to characterize the potential metabolite biomarkers associated with its activity. Present results revealed that naringenin could ameliorate the increases in liver enzymes (ALT and AST) induced by CCl₄ and attenuate the pathological changes in liver tissue. Naringenin decreased urea, creatinine and uric acid levels and improved the kidney tissue architecture, suggesting its role in treating renal disorders. In addition, naringenin increased the expression of the antiapoptoic cell marker, Bcl-2. Significant changes in serum metabolic profiling were noticed in the naringenin-treated group compared to the CCl₄ group, exemplified by increases in palmitic acid, stearic acid, myristic acid and lauric acids and decrease levels of alanine, tryptophan, lactic acid, glucosamine and glucose in CCl₄ model rats. The results suggested that naringenin’s potential hepato- and renoprotective effects could be related to its ability to regulate fatty acids (FAs), amino acids and energy metabolism, which may become effective targets for liver and kidney toxicity management. In conclusion, the current study presents new insights into the hepato- and renoprotective mechanisms of naringenin against CCl₄-induced toxicity.     

Protective role of oligonol from oxidative stress-induced inflammation in C6 glial cell

BACKGROUND/OBJECTIVES

Natural products or active components with a protective effect against oxidative stress have attracted significant attention for prevention and treatment of degenerative disease. Oligonol is a low molecular weight polyphenol containing catechin-type monomers and oligomers derived from Litchi chinensis Sonn. We investigated the protective effect and its related mechanism of oligonol against oxidative stress.

MATERIALS/METHODS

Oxidative stress in C6 glial cells was induced by hydrogen peroxide (H₂O₂) and the protective effects of oligonol on cell viability, nitric oxide (NO) and reactive oxygen species (ROS) synthesis, and mRNA expression related to oxidative stress were determined.

RESULTS

Treatment with oligonol inhibited NO and ROS formation under cellular oxidative stress in C6 glial cells. In addition, it recovered cell viability in a dose dependent-manner. Treatment with oligonol also resulted in down-regulated mRNA expression related to oxidative stress, nuclear factor kappa-B (NF-κB) p65, cyclooxygenase-2 (COX-2), and inducible nitric oxide synthase (iNOS), compared with the control group treated with H₂O₂. In particular, expression of NF-κB p65, COX-2, and iNOS was effectively reduced to the normal level by treatment with 10 µg/mL and 25 µg/mL of oligonol.

CONCLUSIONS

These results indicate that oligonol has protective activity against oxidative stress-induced inflammation. Oligonol might be a promising agent for treatment of degenerative diseases through inhibition of ROS formation and NF-κB pathway gene expression.     

富锗灵芝对四氯化碳诱导大鼠肝损伤保护作用

目的 探讨富锗灵芝胶囊对四氯化碳(CCI₄)所致大鼠肝损伤的保护作用。方法 50只Wistar雄性大鼠,随机分为对照组、模型组、富锗灵芝高、中、低剂量组(分别灌胃给予富锗灵芝胶囊450、230、80 mg/kg),采用CCl₄诱导大鼠急性肝损伤;分别测定血清中谷丙转氨酶(ALT)和谷草转氨酶(AST)活性,肝组织经苏木素-伊红染色,光镜下观察肝组织病理状况,并计算肝损伤指数。结果 与对照组比较,模型组大鼠ALT、AST活性[分别为(258.00±64.81)、(423.60±139.85)IU/L]明显升高,肝脏病变总评分[(194.50±27.71)分]明显升高(P<0.01);与模型组比较,富锗灵芝中、低剂量组大鼠血清ALT、AST活性[分别为(131.30±98.94)、(264.00±187.02)和(138.50±86.08)、(265.70±140.59)IU/L]明显降低(P<0.01),大鼠肝脏病变总评分[分别为(141.40±48.35)和(134.10±25.89)分]明显降低(P<0.01)。结论 富锗灵芝胶囊对CCl4所致大鼠肝损伤具有一定保护作用。     

Protective Effect of a Water-Soluble Carotenoid-Rich Extract of Cordyceps militaris against Light-Evoked Functional Vision Deterioration in Mice

Light-evoked retinal photodamage is considered an important factor contributing to functional vision deterioration and can even lead to light maculopathy or dry age-related macular degeneration. Loss of visual acuity (VA) and visual contrast sensitivity function (VCSF) are the major symptoms of retinal degenerative diseases. Cordyceps militaris is a carotenoid-rich Chinese medicinal fungus with antioxidant, anti-inflammatory, and immunomodulatory functions. C. militaris extract is a natural substance, and its bioactive constituents have been shown to confer health benefits, but their application in retinal tissue and functional vision protection in vivo remain incompletely understood. In the present study, we evaluated the influence of water-soluble, carotenoid-rich C. militaris extracts on the visual performance of light-damaged mouse retinas in vivo, using adult female CD-1^® (ICR) albino mice. We showed that oral administration of this C. militaris extract (10 mg/kg, twice daily) protected the neural retina tissue against light-evoked photoreceptor cell death, reduced Müller cell hypertrophic gliosis, and elevated GSH levels and promoted the recovery of VA- and VCSF-thresholds, especially for high spatial frequency-characterized vision. These results suggest that, probably because of its water-soluble carotenoids, C. militaris extract has the potential to prevent or treat light-induced visual dysfunction.     

丹酚酸对四氯化碳致大鼠肝损伤保护作用

目的 探讨具有特定组成的丹酚酸(SA)对四氯化碳(CCl₄)所致大鼠肝损伤的预防性保护作用及其机制。方法 将健康SD成年大鼠随机分为5组,对照组和模型组给予蒸馏水,各实验组分别用3种不同剂量SA灌胃,2周后以花生油(对照组)或CCl₄(其余各组)腹腔注射,24 h后测定大鼠血清天门冬氨酸氨基转移酶(AST)及丙氨酸氨基转移酶(ALT)、血清和肝组织丙二醛(MDA)、谷胱甘肽(GSH)含量以及超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GSH-Px)活性,并观察肝组织病理变化。结果 模型组大鼠血清AST、ALT值分别为615 U/L和243 U/L,而SA组大鼠AST、ALT分别为348~452和134~181 U/L,活性显著下降(P<0.05)。与模型组比较,当SA剂量为300mg/(kg·bw)时,大鼠血清和肝匀浆中的SOD活性分别上升22.7%和16.7%,MDA含量降低19.3%和30.5%,GSH含量升高9.2%和9.1%,差异均有统计学意义(P<0.05)。实验组和对照组间GSH-Px活性没有显著变化(P>0.05)。模型组大鼠肝脏小叶中心部出现明显点状和灶状坏死,而SA不同剂量组大鼠肝脏病变明显减轻。结论 前期给予适量的SA处理可有效抵抗CCl₄所致大鼠急性肝损伤,其保护作用机制可能与提高大鼠机体抗氧化能力有关。     

Protective Effect of Polysaccharides Isolated from <i>Tremella fuciformis</i> against Radiation-induced Damage in Mice

WTF-B, a type of water-soluble homogeneous polysaccharide, was isolated and purified from Tremella Fuciformis. To investigate the radioprotective effect of WTF-B, we employed a 30-day survival assay. Mice were treated with WTF-B once per day for three consecutive days before 8-Gy gamma irradiation. The treatment groups receiving 54 and 72 mg/kg body weight (b.w.) of WTF-B showed 50% survival post-irradiation. The hematological parameters of the peripheral blood indicated that WTF-B, when administered at doses of 72 mg/kg b.w., significantly restored hemoglobin, white blood cell counts and red blood cell counts by the 14th day and 18th day. In addition, spleen colony forming units (CFU-S), the number of nucleated cells in bone marrow (BMNC) and spleen index were used to investigate the radioprotective effect of WTF-B on the hematopoietic system. The treatment groups receiving WTF-B at 18, 54 and 72 mg/kg b.w. doses presented significantly higher BMNC compared to radiation-only group. The group administered 72 mg/kg b.w. WTF-B presented a significant change in CFU-S compared to the radiation-only group. We also completed micronucleus and chromosome aberration assays to explore genotoxicity. The results of those assays indicated that the number of micronuclei induced by 2-Gy irradiation in a group treated with 72 mg/kg b.w. WTF-B decreased from 30.30‰ to 11.32‰. The chromosomal aberration produced by 3-Gy irradiation in the group receiving 72 mg/kg b.w. WTF-B decreased from 56.01% to 28.13%. The results of the present study indicate a potential use for WTF-B as a radioprotector.     

Protective Effect of Wheat Peptides against Indomethacin-Induced Oxidative Stress in IEC-6 Cells

Recent studies have demonstrated that wheat peptides protected rats against non-steroidal anti-inflammatory drugs-induced small intestinal epithelial cells damage, but the mechanism of action is unclear. In the present study, an indomethacin-induced oxidative stress model was used to investigate the effect of wheat peptides on the nuclear factor-κB(NF-κB)-inducible nitric oxide synthase-nitric oxide signal pathway in intestinal epithelial cells-6 cells. IEC-6 cells were treated with wheat peptides (0, 125, 500 and 2000 mg/L) for 24 h, followed by 90 mg/L indomethacin for 12 h. Wheat peptides significantly attenuated the indomethacin-induced decrease in superoxide dismutase and glutathione peroxidase activity. Wheat peptides at 2000 mg/L markedly decreased the expression of the NF-κB in response to indomethacin-induced oxidative stress. This study demonstrated that the addition of wheat peptides to a culture medium significantly inhibited the indomethacin-induced release of malondialdehyde and nitrogen monoxide, and increased antioxidant enzyme activity in IEC-6 cells, thereby providing a possible explanation for the protective effect proposed for wheat peptides in the prevention of indomethacin-induced oxidative stress in small intestinal epithelial cells.     

复方鳖甲软肝片对大鼠CCl4肝纤维化模型疗效研究

目的研究复方鳖甲软肝片对四氯化碳(CCl4)诱导的大鼠肝纤维化模型的治疗效果.方法 80只SD大鼠,雌雄各半,CCl4和橄榄油14混合后,给大鼠腹部皮下注射,每周2次,每次注射剂量为0.15 mL/100 g,制备肝纤维化模型.制模6周起开始用复方鳖甲软肝片灌胃治疗,每天1次,连续治疗3个月.于治疗前、治疗结束、停药后1个月和2个月每组各处死8只大鼠,切取肝脏作病理切片检测.结果复方鳖甲软肝片起效较慢,与模型组相比,在治疗刚结束时肝纤维化程度略有升高(5.2±4.3 vs 4.7±0.5,P>0.05),停药1个月后肝纤维化程度逐渐减轻(2.4±3.1 vs 6.3±3.1,P<0.05),作用持续至停药后2个月.复方鳖甲软肝片对肝纤维化大鼠肝脏的抗炎作用不十分明显,但具有较为明显的抗脂肪变作用,这种作用起效较慢,停药后1个月才显现出来.结论复方鳖甲软肝片具有抗肝纤维化和抗脂肪变作用.     

姜黄素抑制MMP-2及其抑制因子表达治疗肝纤维化的实验研究

目的:探讨姜黄素抑制肝纤维化的效应及其机制.方法:复制大鼠四氯化碳(CCl4)肝纤维化模型,分别以高、中、低剂量姜黄素处理,检测血清透明质酸(HA)、层粘连蛋白(LN)、三型前胶原(PCⅢ)和四型胶原(Ⅵ.C)水平,检测肝组织纤维化程度和基质金属蛋白酶-2(MMP-2)及其抑制因子组织型金属蛋白酶抑制剂-2(TIMP-2)mRNA表达.结果:CCl4成功诱导肝纤维化大鼠模型,姜黄素治疗能够降低血清肝纤维化指标及肝组织纤维化程度,姜黄素可以抑制CCl4诱导的MMP-2和TIMP-2mRNA表达,并能恢复MMP-2/TIMP-2的动态平衡.结论:姜黄素可以通过减少MMP-2及其抑制因子表达抑制肝纤维化.     

大蒜素对乙醇引起肝损伤的拮抗作用

研究大蒜的有效成分大蒜素对乙醇氧化性肝损伤的影响。结果表明大蒜素（１０ｍｇ／ｋｇｉｇ，ｑｄ×１０）不仅能逆转乙醇所致血清丙氨酸转氨酶和谷胱甘肽Ｓ－转移酶活性的升高，而且能明显增加乙醇肝损伤小鼠肝脏谷胱甘肽含量、谷胱甘肽过氧化物酶、谷胱甘肽还原酶和谷胱甘肽Ｓ－转移酶活性。对乙醇所致肝脏丙二醛含量、超氧化物歧化酶和过氧化氢酶活性的改变则无明显影响。提示大蒜素能拮抗乙醇氧化性肝损伤，其机制与增强肝脏谷胱甘肽抗氧化系统的功能有关     

Effect of the administration of zinc sulfate on hypogonadism and impotence in patients with chronic stable hepatic cirrhosis.

Zinc sulfate was administered in a double-blind manner for 6-8 months to cirrhotic outpatients with impotence and/or hypogonadism. Seven placebo and six zinc-treated patients showed mild symptomatic improvement; however, there was no significant clinical difference between the two groups. Serum zinc levels rose significantly in the zinc-treated group but urinary gonadotropin and serum testosterone levels did not change in either group. Zinc sulfate does not appear to be an effective treatment for sexual dysfunction associated with alcohol-induced hepatic cirrhosis.     

Inhibitory Effect of High Temperature- and High Pressure-Treated Red Ginseng on Exercise-Induced Oxidative Stress in ICR Mouse

As previously reported, high temperature- and high pressure-treated red ginseng (HRG) contain higher contents of phenolic compounds and protect C2C12 muscle cells and 3T3-L1 adipocytes against oxidative stress. This study investigated the effect of HRG on oxidative stress using a mouse model. Our results show that the levels of glutamic oxaloacetic transaminase and glutamic pyruvic transaminase, hepatic malondialdehyde in the HRG group were significantly lower than those of the exercise groups supplemented with commercial red ginseng (CRG) or not supplemented. The muscular glycogen level, glucose-6-phosphate dehydrogenase and lactate dehydrogenase activities of the HGR group were higher than that of the CGR group. Furthermore, the HRG treatment group displayed upregulated mRNA expression of Cu/Zn-SOD and muscle regulatory factor 4. These results indicate that HRG may protect oxidative stress induced by exercise as well as improve exercise performance capacity.