Asian Pacific Journal of Tropical Medicine

673-679

Authors: Satyajit Tripathy, Somenath Roy

Malaria is uncontrolled burden in the world till now. Despite of different efforts to develop antimalarial drug for decades, any anti-malarial drug can able to eradicate completely till now. Many anti-malarial substances are practically ineffectual because of their physicochemical limitations, cytotoxicity, chemical instability and degradation, and limited activities against intracellular parasites. Taking into consideration, the amount of research is going to conduct in the field of nanoparticle based drug delivery systems, lead to new ways of improving the treatment of infectious diseases. The study has focused on the progress and advancement of research on nanotechnology based drug delivery to eradicate the malaria. We like to focus the efficacy of nanotechnology based drug application for the opening out of novel chemotherapeutics in laboratory research, which may show the way to better use with age-old antimalarial drug and may draw the attention of pharmaceutical industries for the improvement and designing of effective anti-malarial drugs in future.

685-692

Authors: Khaled M.M. Koriem, Razmy E. Shahabudin, Rafiq Z. Jamaludin

Objective To evaluate a protective effect of Aristolochia gehrtii (A. gehrtii) leaves to inhibit liver toxicity and apoptosis in Schistosoma malayensis (S. malayensis) infection. Methods Forty male albino mice were divided into four equal groups: group 1 control including non-infected healthy mice and groups 2, 3 & 4 subcutaneously infected with S. malayensis cercariae where groups 3 & 4 pretreated with A. gehrtii leaves (200 mg/kg, bwt) & cinnamoylamide (250 mg/kg, bwt), respectively. Results S. malayensis caused a significant increase in serum AST, ALT, ALP, MDA, NO, bilirubin, urea, creatinine, total cholesterol, LDL, triglycerides, and HDL levels. The pretreatment of A. gehrtii leaves and cinnamoylamide significantly inhibited that increase. On the other hand, S. malayensis induced a significant decrease in serum total protein, albumin, globulin, albumin/globulin ratio, blood SOD and GPx, while A. gehrtii leaves and cinnamoylamide pretreatment increased the above parameters. Treatment with A. gehrtii leaves and cinnamoylamide to S. malayensis infected mice increased p53 expression but decreased bcl-2 expression. These results were supported by histopathological investigations. Conclusions A. gehrtii inhibits liver toxicity and apoptosis in S. malayensis infection and this effect is associated with the major cinnamoylamide ingredient of A. gehrtii leaves.

699-702

Authors: Hidayat Hussain, Ines Kock, Ahmed Al-Harrasi, Ahmed Al-Rawahi, Ghulam Abbas, Ivan R. Green, Afzal Shah, Amin Badshah, Muhammad Saleem, Siegfried Draeger, Barbara Schulz, Karsten Krohn

Objective To evaluate the antimicrobial potential of different extracts of the endophytic fungus Phoma sp. and the tentative identification of their active constituents. Methods The extract and compounds were screened for antimicrobial activity using the Agar Well Diffusion Method. Four compounds were purified using column chromatography and their structures were assigned using 1H and 13C NMR spectra, DEPT, 2D COSY, HMQC and HMBC experiments. Results The ethyl acetate fraction of Phoma sp. showed good antifungal, antibacterial, and algicidal properties. One new dihydrofuran derivative, named phomafuranol (1), together with three known compounds, phomalacton (2), (3R)-5-hydroxymellein (3) and emodin (4) were isolated from the ethyl acetate fraction of Phoma sp. Preliminary studies indicated that phomalacton (2) displayed strong antibacterial, good antifungal and antialgal activities. Similarly (3R)-5-hydroxymellein (3) and emodin (4) showed good antifungal, antibacterial and algicidal properties. Conclusions Antimicrobial activities of the ethyl acetate fraction of the endophytic fungus Phoma sp. and isolated compounds clearly demonstrate that Phoma sp. and its active compounds represent a great potential for the food, cosmetic and pharmaceutical industries.

709-714

Authors: Kittiyod Poovorawan, Salyavit Jitmitrapab, Sombat Treeprasertsuk, Thanunrat Thongmee, Apiradee Theamboonlers, Pisit Tangkijvanich, Piyawat Komolmit, Yong Poovorawan

Objective To report clinical outcomes and viral genotypes of acute symptomatic hepatitis E virus (HEV) infection in Thailand. Methods Forty patients with acute symptomatic HEV infection were recruited during 2009-2013. Clinical, demographic and laboratory data were collected. Diagnosis was accomplished by detection of anti-HEV IgM and/or HEV RNA in the serum or stool. HEV genotypes were classified by direct sequencing of RT-PCR products and phylogenetic analysis. Results The high risk group, comprising immune-compromised, liver cirrhosis and very elderly (>80 years) patients (17 cases), had higher levels of serum alkaline phosphatase at presentation compared with the low risk group. Two fatal cases resulted from acute hepatitis E in the high risk group. Initial clinical presentation did not show statistically significant differences. In six cases (6/40), the virus could be detected in serum or stool by RT-PCR and sequencing. Upon molecular characterization, the viruses were classified as HEV genotype 3f and were in the same cluster as Thai swine HEV. Conclusions Our data showed that acute HEV infection has various clinical presentations and outcomes. Higher levels of serum alkaline phosphatase were observed in high risk patients. All isolated viruses were identified as HEV genotype 3f possibly originating from swine.

720-724

Authors: Qiu-Ran Xu, Xin Liu, Ying-Min Yao, Qing-Guang Liu

Objective To investigate the expression of HSP90 and HIF-1α in human colorectal cancer tissue, the influence of HSP90 and HIF-1α on human colorectal cancer biological behavior and their related factors. Methods The expression of HSP90 and HIF-1α protein in human colorectal cancer as well as normal tissue were detected by immunohistochemical method. Results The positive expression rates of HSP90 and HIF-1α protein in normal human colorectal tissue as well as colorectal cancer tissue were 30% vs. 63.0%, 15.0% vs. 71.7%, respectively. There were significant difference (P=0.035 and P=0.005 respectively). The expression of HSP90 was significantly correlated with the differentiation, Dukes stages and lymph node metastasis (P<0.05), while the expression of HIF-1α was significantly correlated with the Dukes stages and lymph node metastasis (P<0.05). Association analysis showed that the expression of HSP90 protein was significantly correlated with that of HIF-1α protein(P<0.01). Conclusions The expression of HSP90 and HIF-1α protein may be related to the development, metastasis and invasion of human colorectal cancer; and their synergistic effects may participate in the development of the colorectal carcinoma.

730-734

Authors: Chun-Lai Zhang, Yue-Hong Li, Hong-Xia Zhou, Yu-Xin Zhang, Yong-Sheng Wang, Zhi-Yong Zhang, Ling-Li Meng, Xiao-Ming Shang

Objective To explore the protective effects of ginseng mixture on myocardial fibrosis (MF) in rats. Methods A total of 60 Wistar rats were randomly divided into control group without modeling operation, and another 4 groups using subcutaneous injections of isopropyl adrenaline for 10 d to set up the MF model: model group with saline lavage treatment after modeling, captopril group with captopril lavage, ginseng mixture group A and group B with low and high dose mixture treatment respectively. After treatment for 14 d, abdominal aorta and myocardial tissue were extracted to observe the pathological morphological changes and heart weight index in each group. Results The left ventricular weight and heart heavy index of captopril group and group B were significantly lower than that of model group and group A (P<0.05); Model group and group A showed a higher hydroxyproline (Hyp) content in myocardial tissue than the control group and lower catalase (CAT) activity than control group (P<0.05); captopril group and group B showed a lower Hyp content and higher CAT activity compared with group A and model group (P<0.05), a significantly lower level of serum glutathione peroxidase (GSH-PX) and CAT and a higher level of serum creatine kinase, lactate dehydrogenase and H2O2 in model group and group A were observed compared with the control group (P<0.05). A higher level of GSH-PX and CAT and a lower level of creatine kinase, lactate dehydrogenase and H2O2 in captopril group and group B were observed compared with group A and model group (P<0.05); and histopathological examination showed that in captopril group and group B, secretion of collagen fiber was significantly inhibited and myocardial injury was significantly lighter than that of model group. Conclusions Ginseng mixture plays a protective effect on myocardium by inhibiting antioxidant process of MF.

739-743

Authors: Ming-Lei Lang, Ai-Lin Qin, Jian-Min Li, Peng Fu

Objective To investigate the protective effect and mechanism of lithium chloride pretreatment on myocardial ischemia-reperfusion injury (I-RI) in rats. Methods A total of 60 SD rats were randomly divided into control group, model group, lithium chloride intervention group and L-arginine methyl ester + lithium chloride intervention group with 15 in each. The I-RI model was established in model group, the lithium chloride intervention group and L-arginine methyl ester + lithium chloride intervention group by method of seaming along left anterior descending coronary artery myocardial, control group was only opened the chest without seaming, ST-elevation within 2 min was regarded as modeling success. Model group did not adopted any intervention, lithium chloride intervention group was treated with lithium chloride injection 15 mg/kg by jugular venipuncture preoperatively, L-arginine methyl ester + lithium chloride intervention group was treated with intraperitoneal injection of 30 mg•kg−1•d−1 L-arginine methyl ester 7 d before the test, and intravenous catheter of 15 mg/kg lithium chloride preoperatively. The hydroxybutyric acid dehydrogenase (HBDH), creatine kinase isoenzyme (CK-MB), superoxide dismutase (SOD), malondialdehyde (MDA) level and nitric oxide synthase (NOS) activites were tested. Each large area of myocardial ischemia tissue was extracted for determination of the MDA content, SOD activity in tissue and serum, and morphological changes of myocardial tissue. Results SOD activity was highest in lithium chloride intervention group, followed by L-arginine methyl ester + lithium chloride intervention group, control group and model group (P<0.05); SOD activity was highest in L-arginine methyl ester + lithium chloride intervention group intervention group, followed by lithium chloride intervention group, control group and model group (P<0.05). MDA content of myocardial tissue was highest in model group, followed by L-arginine methyl ester + lithium chloride intervention group, the lithium chloride intervention group and control group (P<0.05); serum MDA content was highest in L-arginine methyl ester +lithium chloride intervention group, followed by model group, lithium chloride intervention group and control group (P<0.05). Compared with the control group, serum NOS was significantly higher in model group, lithium chloride intervention group and L-arginine methyl ester + lithium chloride intervention group (P<0.05), there was no statistical difference of serum NOS activity between the three groups (P>0.05); HBDH and CK-MB of plasma were highest in model group, followed by L-arginine methyl ester + lithium chloride intervention group, lithium chloride intervention group and control group (P<0.05). A significantly lighter myocardial damage was observed microscopically in lithium chloride intervention group than that in L-arginine methyl ester + lithium chloride intervention group and model group. Conclusions lithium chloride pretreatment can significantly reduce the myocardial I-RI, maintain structure and function of myocardial cells, improve the antioxidant ability of myocardial tissue, play an effective role on protecting myocardial I-RI.

749-753

Authors: Shu-Jie Zhao, Shi-Ji Wang, Hong-Xiang Li, Li-Hua Dong, Huai-Jiang He, Zhong-Min Liu, Yu-Shan Wang

Objective To tinvestigate the protective effect and mechanism of emodin pretreatment on intestinal mucosa of rats with intestinal ischemia-reperfusion injury. Methods A total of 50 SD rats were randomly divided into control group, model group, emodin groups of low, medium and high dose, with 10 in each group. Ischemia-reperfusion injury (I-RI) mode was established by using noninvasive clamp on superior mesentericartery (SMA). Control group and model group were pretreated with 0.5% sodium carboxymethyl cellulose solution lavage 2 h before operation, emodin groups of low, medium and high dose were given emodin lavage with 20, 40, 60 mg/kg pretreatment, femoral venous blood before the lavage pretreatment (T0) and 1 h ischemia (T1), and inferior vena venous blood after 1 h of reperfusion (T2) were extracted from each group of rats for detection of serum level of intestinal fatty acid binding protein (I-FABP), tumor necrosis factor (TNF-α), endotoxin, interleukin 6 (IL-6), and the content of diamine oxidase (DAO); After model establishment, the rats were sacrificed, intestine homogenate was prepared by using blind intestinal tissue to detect intestinal tissue myeloperoxidase (MPO), malondialdehyde (MDA) and superoxide dismutase (SOD) levels. And upper small intestine tissue was retrieved, followed by fixation and conventional HE staining to observe intestinal tissue morphology under light microscopy. Results In emodin groups of low, medium and high dose at T1 and T2, I-FABP, TNF-α, endotoxin, IL-6 and DAO level were significantly lower than that of model group (P<0.05); in emodin group of low, medium and high dose, MPO and MDA content in intestinal tissue homogenate was significantly lower than that in model group (P<0.05), SOD level was significantly higher than that of model group (P<0.05). Intestinal damage of emodin low, medium and high dose groups were significantly lighter than model group. Conclusions Emodin pretreatment has certain protective effect on intestinal mucosa in ischemia reperfusion injury.