Biology subjects

Pandey, H.

Publications and source records attributed to Pandey, H..

5 recordsLinked to original sources

bioRxiv2019

Nutritive diet becomes unhealthy if taken in a wrong ratio: Scientific validation of Ayurvedic concept of \"incompatible diet\" (Virrudh Aahar)

Honey and ghee is an important constituent of our diet. Honey contain about 200 components in its which play an important role as antioxidative, anti-inflammatory, antimicrobial, wound healing and sunburn, etc. Ghee has also many essential constituents such as phospholipids, PUFA, fat- soluble vitamins, etc. It is mention in Charak Samhita that equal ratio of honey and ghee when taken in food become toxic to health. This study was designed to explore the mechanism of toxicity through the biochemical and histological parameter. For this study, 24 Charles foster rats were taken and divided into four groups (n=6) normal, honey, ghee, and honey+ghee (1:1). After 60 days rats were sacrificed. Weight loss, Hair loss and red patches on ear were found on honey+ghee fed rats. LFT, amadori test, AGE, UV, glucose, DPP-4 and LPO were found significantly increased in honey+ghee group. SOD, Catalase, GSH, ABTS+, GLP-1, GIP-1, ACB and HB were found significantly decreased in honey+ghee group. No changes were found in RFT. H&E show normal morphology in kidney, intestine, and pancreas but mild inflammation was found in liver tissue. We conclude that the equal mixture of honey and ghee shows toxic effect. Increased formation of hydroxymethyl furfural, amadori product, DPP-4 activity and low incretins (GLP-1, GIP-1) activity resulting high postprandial hyperglycemic response are collectively responsible for oxidative stress-mediated toxicity of the mixture of honey and ghee in equal ratio.

pharmacology and toxicology↗

bioRxiv2019

Histopathological study of different organs of charles foster strain rat under the exposure of Pueraria tuberosa.

The present study was undertaken to investigate the safe doses of Pueraria tuberosa water extract (PTWE) on different organs. The OECD guidelines 407 of repeated toxicity was followed with respect to the selection of dose and days for different organs. The selected doses of PTWE were 250, 500, 1000 and 2000 mg/kg b wt for 7, 14, 21 and 28 days. Haematoxylin and eosin staining was used to study the morphological alterations in heart, intestine, testis, adrenal gland and spleen. In the present study, no adverse alterations in cardiac fibers of the heart, size and shapes in crypts and villi of intestine, seminiferous tubules and spermatozoa count in testis, three zones of adrenal gland, and spleen were seen in all treated groups of PTWE. There were no adverse morphological alterations found in described organs. The PTWE are safe at 1000 mg/kg b wt. up to 28 days and 2000 mg/ kg b. wt up to 21 days, respectively.

pharmacology and toxicology↗

bioRxiv2019

Herbal tablet of Pueraria tuberosa water extract suppresses the alloxan induced liver damage and hyperglycemia in rats

AimTo study the protective response of herbal formulation (tablets) of Pueraria tuberosa water extract (PTAB) on alloxan induced rat diabetic model.\n\nMethodologyAlloxan (120 mg/kg bw) was injected intraperitonially. Rats were divided into three groups: group 1 as normal, group 2 as diabetic control and group 3 were given PTAB upto 14 days. Blood glucose and liver function tests were done using their respective kits. Hematoxylene and eosin staining was done to evaluate the morphological changes in liver tissues. Through immunohistochemistry, we have checked the protein expression of VEGF, MMP9 and ki67.\n\nResultPTAB significantly decreases blood glucose level in a time dependent manner up to 14 days. As compared to diabetic control, PTAB decreases SGOT, SGPT and alkaline phosphates after 14 days of treatment. In diabetic control, the morphology of liver tissues were found damaged due to deformed hepatocytes and dilated lobules. Most of the hepatocytes after PTAB treatment were comparatively found similar to normal rats tissues, along with dilated blood vessels and normalized liver lobules. In addition to these results, PTAB suppresses the expressions of VEGF and MMP 9.\n\nConclusionPTAB was found to act as an effective hypoglycemic agent. In addition to this, PTAB also found to inhibit inflammation and apoptosis of liver. Thus, can be taken as a potential drug in liver diseases.

pharmacology and toxicology↗

bioRxiv2019

Anti-oxidant, anti-apoptotic, anti-hypoxic and anti-inflammatory conditions induced by PTY-2 against STZ-induced stress in islets

Background and AimEarlier assessment of Pueraria tuberosa tubers has shown anti-diabetic effects through incretin mimetic action and DPP-IV inhibition. The aim of this work was to further explore the protective role of aqueous extract of Pueraria tuberosa against streptozotocin (STZ)-induced pancreatic stress in rats.\n\nMethodsDiabetes was induced with STZ (65 mg/kg body weight) in Charles foster male rats. After 60 days of STZ administration, animals with blood glucose levels > 200 g/dL were considered as diabetic. All the rats were later divided into three groups: Group-1 (STZ untreated normal rats), Group-2 (Diabetic control), and Group-3 (PTY-2 [50 mg/100 g bw treatment for next 10 days to diabetic rats). The rats were then sacrificed at the 10th day of treatment accordingly.\n\nResultsSTZ treatment led to an increase in expression of MMP-9, Tnf , HIF-1, VEGF, IL-6, PKC {varepsilon}, NF-kB, and Caspase-3. Reverse transcriptase Polymerase Chain Reaction (PCR), IHC and western blot analysis showed an increase in the expressions of superoxide dismutase (SOD) and Nephrin, and a decrease in the expressions of NF-kB, PKC {varepsilon}, TNF- MMP-9, HIF-1, VEGF, Caspase 3 and IL-6 after 10 days of PTY-2 treatment.\n\nConclusionThe results show that PTY-2 favorably changed the expression of NF-kB, PKC {varepsilon}, TNF , MMP 9, HIF-1, VEGF, IL-6, Caspase3, Nephrin and SOD in cases of STZ-induced pancreatic stress. Further evaluation of PTY-2 might be helpful in establishing its role in the management of diabetes mellitus.\n\nHighlightsO_LIPTY 2 act as a protective herbal drug against STZ induced islet stress.\nC_LIO_LIPTY 2 upregulates protective and downregulates harmful markers.\nC_LIO_LIThis study composed of four pathway through which PTY 2 acts on pancreas.\nC_LI\n\nGRAPHICAL ABSTRACT\n\nO_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=156 SRC=\"FIGDIR/small/670364v1_ufig1.gif\" ALT=\"Figure 1\">\nView larger version (69K):\norg.highwire.dtl.DTLVardef@14b1f18org.highwire.dtl.DTLVardef@e6a1f2org.highwire.dtl.DTLVardef@19225b0org.highwire.dtl.DTLVardef@1e87bf5_HPS_FORMAT_FIGEXP M_FIG Mechanism of action of PTY 2 against STZ induced islet stress.\n\nC_FIG

pharmacology and toxicology↗

bioRxiv2019

PTY 2 As DPP-IV Inhibitor Prevents Intestinal Cell’s Apoptosis

Enhanced DPP-IV expression is found to get enhanced in various intestinal diseases. PTY-2 has already been known to have DPP-IV inhibitory potential. This inhibition has not yet been studied at mRNA level. Increased incretin secretion due to DPP-IV inhibition could lead to suppression of stress & intestinal cells apoptosis. Through histological analysis, we have found morphological damage of intestine after STZ injection (65 mg/kg bw) to male Charles foster rats. mRNA expressions were analyzed by PCR and apoptosis of cells was checked through tunnel assay & Bcl 2 expression. The number and length of villi get reduced in STZ induced diabetic control, but these damages have been getting reversed after the PTY-2 treatment for 10 days. The expression of SOD was found to get reduced while that of DPP-IV was enhanced in diabetic control group along with significant intestinal cell apoptosis. PTY-2 treatment reduces the stress by upregulating the expression of SOD and through downregulation of DPP-IV mRNA expression. These recoveries by PTY-2 leads to suppression of intestinal cells apoptosis. These short studies explain the protective action of PTY-2 against STZ induced intestinal damage. Hence, PTY-2 could be taken as an herbal treatment against intestinal disorders in case of chronic diabetes.

pharmacology and toxicology↗