Curcumin effect on Bleomycin-induced pulmonary fibrosis in Mus musculus

Curcumin, a curcuminoid compound of turmeric has been demonstrated to have anti-oxidant and anti-inflammatory properties. Bleomycin (BLM) is an anti-cancer drug induced pulmonary fibrosis in human and animals. This study was aimed to investigate biological effects of curcumin on bleomycin-induced pulmonary fibrosis in mice (Mus musculus) through pathomorphological assessment. In this study, 16 mice ddy strain were divided into four groups, namely (i) control, mice were subcutaneously (SC) injected with 100 µl sterilized aquadest in dorsal skin, (ii) BLM group, injected SC with 100 µl of 1 mg/ml BLM in dorsal skin, (iii) Curcumin (CMN) group, mice were intraperitoneally (IP) injected with 100 mg/kg body weight (BW) curcumin dissolved in 0,5% carboxy methyl cellulose (CMC) and injected with 100 µl sterilized aquadest SC, (iv) BLM+CMN group, injected SC with 100 µl of BLM 1 mg/ml and injected IP with 100 mg/kg BW CMN in 0,5% CMC. All treatments were performed daily for four weeks period. The lung samples were collected and fixed in buffered neutral formalin (BNF) 10%. Histopathological evaluation was performed with hematoxylin-eosin (HE) and Masson’s trichrome (MT) stains. The results showed that BLM treatment significantly increased fibrosis area and alveolar wall area fraction as compared to control. OIn the other hand, CMN treatment significantly reduced fibrosis area and alveolar wall area fraction in mice treated with BLM. In conclusion, our study showed that CMN treatment may inhibit lung fibrogenesis in BLM-induced pulmonary fibrosis

PAT-4 Histopathological Study of Mice (Mus musculus) Digestive Organs Treated with Alkali pH Water

Water is an important part of the body. As much as 50-60% of an adult's body weight consists of water. Water functions in the body include as a means of transporting substances, regulating body temperature, regulating body pH, forming body structures, solvents for the body's chemical reactions, and helping the body's mechanical functions, such as lubrication (Insel et al. 2004; Asamadi 2008). In the event of water deficiency, the body will become dehydrated which able to cause cell death to individual death (Stanfield and Hui 2008). Recently, there are alkaline pH drinking water products that are commercially popular that have pH around 8-10 (alkaline water). Some parties claim that alkaline water can help neutralize the level of acidity (pH) of blood due to free radicals, while also having micro cluster technology that can increase oxygen solubility. According to Shirahata et al. (2012) alkaline water is beneficial for health because it can suppress oxidative stress.This study aims to know the effect of alkaline pH drinking water reviewed through histopathological studies of the digestive organs of mice (stomach, intestine, and pancreatic exocrine glands)

PF-18 Photomicrograph of Nanogel Andrographolide-Beta Cyclodextrine Inclusion Complex As Anti-Burns

Inclusion complex is a complex formed between drug molecules which act as guest or located inside the cavity of host molecule. Host molecules are commonly originated from the derivative group of cyclodextrin. Among cyclodextrin groups, beta cyclodextrin (BCD) is mostly used in formula development and drug delivery system [1].Andrographolide (AG) is a pure isolate chemically syntesized from sambiloto herbs (Andrographis paniculata Nees), in the form of needle cystal-like which is colorless and extremely bitter. AG has variety of medical properties, particularly as anti-inflamation to treat skin burns [2]. However AG has poor solubility in water. This will result in low abillity to solute, penetrate membrane, and distribute the drug when applied transdermally in burn skin. In burn skin, there is tendency to skin damage, especially in stratum corneum which acts as semipermeable barrier. The ability of drugs that applied transdermally tends to be high.Formation of inclusion complex using AG and BCD to increase the ability of AG in penetrating membrane should be done. Transmission Electron Microscope (TEM) is a fast technique to confirm the formation of drug or inclusion complex by  comparing the shape and particle size [3]. Study on percutaneous penetration of AG-BCD inclusion complex is produced through solvent evaporation method at mole ration 1:2 in viscolam gel preparation

Efek Protektif Andrografolid terhadap Kejadian Kardiotoksisitas Pasca Aplikasi Doksorubisin pada Tikus

Cardiotoxicity is one of the important side effects of doxorubicin, an anthracycline antibiotic and chemotherapeutic drug. The aim of this study was to explore the potential protective effect of andrographolide (Andro), an anti-inflammatory and anti-oxidant agents, against cardiotoxicity induced by doxorubicin (DXR). Thirty Sprague Dawley rats (80-100 g) were divided into four groups: (a) Control (b) DXR (4 mg/kg intraperitoneally (IP) were made weekly for 4 weeks), (c) DXR+Andro20 (low dose andro; 20 mg/kg IP weremade daily for 4 weeks, 24 h after DXR), (d) DXR+Andro100 (high dose andro; 100 mg/kg IP were made daily for 4 weeks, 24 h after DXR). Furthermore, at the end of experimental period, all rats were euthanized and hearts were removed for hispatological analyses. Hematoxylin-eosin (HE) and Masson Trichrome (MT) staining were used to observe the histomorphological alterations and fibrosis of hearts, respectively. Our results showed that andrographolide treatment (20 mg/kg) augmented the detrimental effects of DXR such as decreased body weight and heart weight, as compared with those in DXR-treated rats. Histopathologically, heart tissue from control group showed compact myocardial architecture without any noticeable lesions. Histopathological analysis fromDXR group showed severe inflammation and fibrosis, whereas DXR+Andro20 group showed almost normal heart morphology. Andrographolide at a dosage of 100 mg/kg did not show protective effects against doxorubicin,and even aggravated myocardial inflammation, as compared with DXR-treated rats. These results indicate that low dose of andrographolide compromised doxorubicin-induced decreased body weight, heart inflammation, andfibrosis

Potential Deleterious Effects of L-Citrulline Supplementation in Isoproterenol-Induced Myocardial Infarction: Focus on Nitrosative Stress

L-Citrulline shows potential activity as a supplement to prevent myocardial infarction through vasodilative and possible antioxidative effects but may be deleterious by causing nitrosative stress. This study determined the potentially deleterious effects of L-citrulline supplementation in isoproterenol-induced myocardial infarction with a focus on nitrosative stress. L-Citrulline supplementation was given orally at dosages of 300 or 600mg/kg body weight daily for 6 days. Myocardial infarction was induced in Wistar rats via subcutaneous injection of isoproterenol (85 mg/kg body weight (BW)) on day 4 and 5. Blood pressure was measured at the end of the study (day 6) and rats were sacrificed to collect heart tissue samples for a histopathological evaluation. The histopathological evaluation was done using hematoxylin and eosin staining for the myocardial damage evaluation and immunohistochemical (IHC) staining of arginase-2, inducible nitric oxide synthase (iNOS), and 3-nitrotyrosine to evaluate nitrosative stress. L-Citrulline supplementation failed to show a significant protective effect on blood pressure and exacerbated the decrease of diastolic blood pressure. Both low and high dose L-citrulline supplementation had a significant protective effect on myocardial damage compared to the isoproterenol group (p<0.01). L-Citrulline also caused increased nitrosative stress as shown by increased expression of arginase-2 and 3-nitrotyrosine on IHC staining but tended to show an ameliorative effect on iNOS expression. A significant increase in arginase-2 expression was detected between the high dose group and the other groups (p<0.01 vs. normal and isoproterenol groups; p<0.05 vs. low dose group). L-Citrulline supplementation increased 3-nitrotyrosine expression in a dose-dependent manner, which was significantly different compared to the normal group (low dose: p<0.013; high dose: p<0.003). L-Citrulline increased the production of nitrosative stress but resulted in less myocardial damage through its other effects

Pathology of cutaneous blastomycosis in a cat

Cats are common as pet animals in Indonesia and live in close vicinity of human neighborhood, which make them potential for transmitting diseases to human. Blastomycosis is infectious disease caused by Blastomyces spp yeast. Here we describe morphopathology of blastomycosis found in skin of a Persian Cat. Grossly, the lesion were characterized by ulcerated wounds and multiple subcutaneous small nodules (2-5 mm in diameter) in the base of tail. Skin biopsy was made and further processed for histopathology.  Microscopically, the lesion consist of epidermal necrosis, dermatitis, with coalescing dermal granulomatous inflammation, characterized by epitheloid and foreign type giant cells infiltrates. Numerous spherical-shaped structures and pseudohyphae which are Periodic Acid Schiff (PAS)-positive consistent with yeast morphology were found within the granulomas; morphology is also consistent with Blastomyces spp yeasts. Conclusively, multiple granulomatous dermatitis with evidence of Blastomyces yeasts is a hallmark of cutaneous blastomycosis. Exposure to Blastomyces spp yeast may possess infection threat to pet owners

The Effect of Mangiferin Against Brain Damage Caused by Oxidative Stress and Inflammation Induced by Doxorubicin

Doxorubicin (DOX) is an anthracycline antibiotic used for anticancer therapy. However, this agent can cause various systemic side effects including cognitive impairments in chronic use. Brain damage due to DOX is caused by an increase of tumor necrosis factor-alpha (TNF-α) level in the brain. Increased TNF-α can further lead to chronic inflammation which can lead to neuronal deaths or neurodegenerative diseases. Mangiferin (MAG), a compound extracted from Mangifera indica, has been found neuroprotective activities, but its effect on DOX-induced brain damage is unknown. This study aims to determine the effect of MAG on brain damage induced by DOX. Male Sprague-Dawley rats were induced by DOX intraperitoneally. MAG was given orally at the doses of 30 and 60 mg/kg bw for 7 consecutive weeks. The parameters measured were inflammatory and oxidative stress markers in brain tissue. Coadministration of MAG with DOX reduced inflammation which was marked by the reduction of TNF-α mRNA expression, decreased TNF-α level and reduction of oxidative stress marked by increase of superoxide dismutase level and decrease of malondialdehyde level. In conclusion, MAG was shown to have a neuroprotective effect on brain damage induced by DOX, partly due to inhibition of inflammation and oxidative stress

Relationship of Cell Proliferating Marker Expressions with PGE2 Receptors in Regenerating Rat Renal Tubules after Cisplatin Injection

Cisplatin, an anticancer drug, is well known to have nephrotoxicity as an adverse effect. We investigated the expressions of cell cycle markers and prostaglandin E2 (PGE2) receptors (EP) in the affected renal tubules in rats injected with a single dose (6 mg/kg body weight) of cisplatin. On days 1–3 after dosing, the affected renal epithelial cells were almost desquamated, showing necrosis. On day 5 onwards, the renal tubules were rimmed by flattened or cuboidal epithelial cells with basophilic cytoplasm; BrdU-immunopositive cells began to significantly increase, indicating regeneration. Simultaneously, TUNEL-positive apoptotic cells were also seen. On days 1–5, cyclin D1-immunopositive cells were decreased with an increased expression in p21 mRNA, indicating G1 arrest in the cell cycle. The affected renal epithelial cells began to react to EP4 receptor, but not to EP2 receptor. Some EP4 receptor-reacting epithelial cells gave a positive reaction to BrdU or cyclin D1. Collectively, the affected renal tubules underwent various alterations such as necrosis, apoptosis, regeneration and G1 arrest; the aspects might be influenced by endogenous PGE2 through EP4 receptor

Efek Protektif Andrografolid terhadap Kejadian Kardiotoksisitas Pasca Aplikasi Doksorubisin pada Tikus

Cardiotoxicity is one of the important side effects of doxorubicin, an anthracycline antibiotic and chemotherapeutic drug. The aim of this study was to explore the potential protective effect of andrographolide (Andro), an anti-inflammatory and anti-oxidant agents, against cardiotoxicity induced by doxorubicin (DXR). Thirty Sprague Dawley rats (80-100 g) were divided into four groups: (a) Control (b) DXR (4 mg/kg intraperitoneally (IP) were made weekly for 4 weeks), (c) DXR+Andro20 (low dose andro; 20 mg/kg IP were made daily for 4 weeks, 24 h after DXR), (d) DXR+Andro100 (high dose andro; 100 mg/kg IP were made daily for 4 weeks, 24 h after DXR). Furthermore, at the end of experimental period, all rats were euthanized and hearts were removed for hispatological analyses. Hematoxylin-eosin (HE) and Masson Trichrome (MT) staining were used to observe the histomorphological alterations and fibrosis of hearts, respectively. Our results showed that andrographolide treatment (20 mg/kg) augmented the detrimental effects of DXR such as decreased body weight and heart weight, as compared with those in DXR-treated rats. Histopathologically, heart tissue from control group showed compact myocardial architecture without any noticeable lesions. Histopathological analysis from DXR group showed severe inflammation and fibrosis, whereas DXR+Andro20 group showed almost normal heart morphology. Andrographolide at a dosage of 100 mg/kg did not show protective effects against doxorubicin, and even aggravated myocardial inflammation, as compared with DXR-treated rats. These results indicate that low dose of andrographolide compromised doxorubicin-induced decreased body weight, heart inflammation, and fibrosis