Search

Heat shock proteins (HSPs), which function as chaperones, are activated in response to various environmental stressors. In addition to their role in diverse aspects of protein production, HSPs protect against harmful protein-related stressors. Calycosin exhibits numerous beneficial properties. This study aims to explore the protective effects of calycosin in the heart under heat shock and determine its underlying mechanism. H9c2 cells, western blot, TUNEL staining, flow cytometry, and immunofluorescence staining were used. The time-dependent effects of heat shock analyzed using western blot revealed increased HSP expression for up to 2 h, followed by protein degradation after 4 h. Hence, a heat shock damage duration of 4 h was chosen for subsequent investigations. Calycosin administered post-heat shock demonstrated dose-dependent recovery of cell viability. Under heat shock conditions, calycosin prevented the apoptosis of H9c2 cells by upregulating HSPs, suppressing p-JNK, enhancing Bcl-2 activation, and inhibiting cleaved caspase 3. Calycosin also inhibited Fas/FasL expression and activated cell survival markers (p-PI3K, p-ERK, p-Akt), indicating their cytoprotective properties through PI3K/Akt activation and JNK inhibition. TUNEL staining and flow cytometry confirmed that calycosin reduced apoptosis. Moreover, calycosin reversed the inhibitory effects of quercetin on HSF1 and Hsp70 expression, illustrating its role in enhancing Hsp70 expression through HSF1 activation during heat shock. Immunofluorescence staining demonstrated HSF1 translocation to the nucleus following calycosin treatment, emphasizing its cytoprotective effects. In conclusion, calycosin exhibits pronounced protective effects against heat shock-induced damages by modulating HSP expression and regulating key signaling pathways to promote cell survival in H9c2 cells. [ABSTRACT FROM AUTHOR]

Elimination of synthetic azo dyes of textile industrial effluents still being a great challenge worldwide as it engenders several hazardous effects in the ecosystem. Bioremediation technology has remarkable potential to approach this kind of problem due to its environmentally friendly and economical nature. Ligninolytic enzyme systems seem to have shown great potential to degrade a variety of recalcitrant pollutants and xenobiotic compounds including dyes. This study aimed to isolate and identify ligninolytic bacterial consortium from Western Ghats foothill soil with the potential to degrade azo dyes. Nine ligninolytic bacterial strains were isolated from soil samples. All the strains were able to decolorize a mixture of azo dyes (DR 23, DB 15 and DY 12). Three potential strains with maximum dye decolorizing efficiency were selected and identified by 16S rRNA gene sequencing studies. The influence of bacterial monocultures and mixed cultures in the dye decolorization was studied with the selected strains. Three monocultures and four mixed cultures were developed and studied for their ability to decolorize MSM containing 200mg/l of azo dye mixture. The ligninolytic bacterial consortium WGC-D was found to be more effective which decolorized up to 75% of dye. The mechanism of dye decolorization was assessed by spectral studies. The changes in the UV spectrum of bacterial consortium treated and untreated samples validated that the mechanism of the decolorization process was biodegradation. The consortium removes 89% of COD and 84% of color from textile industrial effluent. The results reveal that the ligninolytic bacterial consortium could be useful as a candidate in the secondary screening process in the textile dye effluent treatment in industries.

Abstract Background Sunitinib is a multiple receptor tyrosine kinase inhibitor (TKI) used for the treatment of renal cell carcinoma (RCC). It increases the median survival considerably with minimum side effects. Alopecia is one of the rare side effects. Metastasis to the ovary is also rare. We report a case of RCC metastasizing to the ovary developing alopecia early on starting sunitinib. Case presentation A 22-year-old hypothyroid girl underwent right radical nephrectomy for T2N0 RCC. Histopathology was clear cell carcinoma. Six months later, she presented with right iliac fossa pain, imaging revealed metastasis to the ileocolic junction and the ovary, an exploratory laparotomy was carried out and, after debulking, the patient was started on sunitinib. Four weeks after the start of the treatment, she developed alopecia. She was continued with sunitinib therapy till progression. Conclusions The present case shows a rare metastasis to the ovary and early onset of rare adverse event of alopecia on starting sunitinib therapy. In the presence of confounding factors like hypothyroidism and dandruff, establishing this as an adverse reaction of sunitinib is difficult. This case had a unique metastatic spread with involvement of the bowel, ovary and peritoneal carcinomatosis. Use of adjuvant TKI's after resection of primary tumour in nonmetastatic setting may reduce metastatic rates and increase progression-free survival.

Tetrahydrobiopterin (BH4) is an essential biological cofactor and a derivative of pterin which is considered potent anticancer agents. In continuation of our previous study on the identification of BH4 from cyanide‐degrading Bacillus pumilus, the present study focuses on evaluating the anticancer properties of BH4 on A549, a human lung adenocarcinoma. Anticancer activity analysis shows that BH4 inhibited A549 cell growth after 24 h of incubation with 0.02 mg/mL. In acridine orange/ethidium bromide staining, BH4‐treated A549 cells showed apoptotic morphology. BH4 treatment caused cell cycle arrest at G0/G1 phase compared to control cells. BH4 augmented p53 expression in alveolar cancer cells by downregulating MDM2 levels. There was downregulation of casp‐3 and upregulation of iNOS gene in BH4‐treated A549 cells. Further, docking studies indicated that BH4 had significant interactions with the above proteins affirming the apoptosis mechanism. Thus, BH4 could be considered a potential anticancer drug. [ABSTRACT FROM AUTHOR]